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QH371 

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371 

L3 


THIS  BOOK  IS  DUE  ON  THE  DATE 
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EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA 

CONCERNING  EVOLUTION. 


BY 


FRANK  E.  LUTZ 


PUBLISHE 


:*  BY  TH 


WASHINGTON,  u.  c. 
e  Carnegie  Institution  of  Washington 
1911 


North  Carolina  State  Library 


Gift  of 


North 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA 
CONCERNING  EVOLUTION. 


BY 


FRANK  E.  LUTZ 


WASHINGTON,  D.  C. 
Published  by  the  Carnegie  Institution  of  Washington 

1911 


CARNEGIE  INSTITUTION  OF  WASHINGTON,  PUBLICATION  No.  143 


Paper  No.  16  of  the  Station  for  Experimental  Evolution  at 
Cold  Spring  Harbor,  New  York 


Copies  of  this 
were-  first  issued 

MAR  14 1911 


the  cornman  printing  CO. 

CARLISLE,  PA. 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


THE  INHERITANCE  OF  ABNORMAL  VENATION. 

THE  EFFECT  OF  SEXUAL  SELECTION. 

DISUSE  AND  DEGENERATION. 


in 


THE  INHERITANCE  OF  ABNORMAL  VENATION. 


Practically  all  the  experimental  studies  of  inheritance  have  extended 
through  but  few,  rarely  more  than  6,  generations  and  have  been  con- 
cerned with  pairs  of  non-intergrading  characters.  In  the  present  work 
more  than  70  generations  have  been  reared.  This  was  possible  for  two 
reasons:  Drosophila  ampelophila  Loew  has  a  very  short  life-history, 
and  it  can  be  kept  breeding  throughout  the  year.  The  character 
abnormal  wing-venation,  the  inheritance  of  which  was  studied,  may 
be  made  to  exhibit  extreme  variability,  passing  from  less  venation  than 
normal  through  normal  to  extra  venation,  so  great  that  the  additional 
veins  almost  equal  the  normal  in  extent. 

At  the  Boston  (1907)  meeting  of  the  International  Zoological  Congress 
a  preliminary  report  was  presented  upon  this  subject,  6  generations 
having  been  obtained.  During  the  summer  of  1908  a  report  upon  the 
work  (covering  about  25  generations)  done  at  the  Station  for  Experi- 
mental Evolution  was  submitted  to  the  Director,  but  I  deferred  publi- 
cation because  I  wished  to  test  more  in  detail  certain  points,  especially 
sexual  selection  and  the  further  fate  of  the  abnormal  strains.  This 
additional  work  was  done  at  the  American  Museum  of  Natural  History. 
Incidentally  I  obtained  confirmation  of  the  previous  work,  but  for  the 
most  part  the  present  paper  includes  only  the  Cold  Spring  Harbor  data 
and  the  conclusions  drawn  are  as  given  in  the  1908  report,  except  where 
otherwise  indicated. 

MATERIAL  AND  METHODS. 

Drosophila  ampelophila  (the  small  red-eyed  "pomace-fly")  is  very 
common  about  cider-mills,  ripe  fruit,  vinegar-barrels,  and  the  like. 
The  larvae  normally  live  in  the  pulp  of  rotting  fruits,  especially  during 
the  acetic-acid  stage  of  decay.  They  will,  however,  thrive  on  the  side 
of  a  tumbler  containing  fruit-juices,  and  I  have  reared  them  through 
several  generations  on  stale  beer.  At  a  temperature  of  25°  C.  the  eggs 
hatch  in  40  hours  or  less.  The  duration  of  the  larval  period  is,  on  the 
average,  5  days,  2nd  of  the  pupal  period  4§  days.  The  adults  become 
sexually  mature  about  48  hours  after  emergence  when  kept  at  this  tem- 
perature. They  live  for  about  3  weeks.  The  mean  number  of  eggs  is 
close  to  200.     Copulation  is  repeated  and  frequent. 

Most  of  the  flies  discussed  in  this  paper  were  bred  in  an  incubator, 
where  an  average  temperature  of  25.5°  C.  was  maintained.  A  thermo- 
graphic record  was  kept.  Since  the  temperature  of  the  incubator  was  so 
nearly  that  of  the  working-room,  absolute  constancy  was  not  obtained. 

The  amount  of  variation  is  shown  in  fig.  1,  which  gives  the  frequencies 

l 


2  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

of  the  different  degrees  as  found  during  four  typical  months  from  read- 
ings of  the  thermogram  at  3-hour  intervals.  For  the  purpose  of  these 
experiments  even  this  approximation  to  constancy  does  not  seem  neces- 
sary, as  variations  of  temperature  were  found  to  have  no  influence  upon 
the  wing-venation.  Therefore  the  incubator  was  not  used  in  the  latter 
part  of  the  work. 


Class  18.33 

Frequency  o 


Fig.  1. 


Bananas  were  used  as  food.  They  were  purchased  while  still  quite 
green  and  ripened  in  glass-stoppered  bottles.  In  this  way  accidental 
introduction  of  wild  flies  was  rendered  unlikely.  Even  had  Drosophila 
eggs  been  laid  on  the  green  banana,  they  would  have  hatched  and  the 
larvae  would  have  developed  into  plainly  visible  pupae  before  the  banana 
was  used.  Frequent  control-cultures  were  kept  and  in  no  case  was  a 
Drosophila  found  in  them.  The  flies  with  their  food  were  kept  in  care- 
fully washed  glassware  and  the  instruments  used  in  handling  the  food 
were  sterilized  in  an  alcohol  flame  after  every  operation  which  could 
possibly  get  eggs  or  larvae  upon  them.  The  importance  of  this  caution 
can  not  be  too  strongly  urged  upon  those  who  carry  out  pedigree- work 
with  this  insect. 

An  egg-laying  female  was  given  a  fresh  piece  of  banana  every  two  days 
and  an  effort  was  made  to  have  all  the  banana  of  the  same  degree  of 
decay.  Each  piece  was  kept  separate  during  the  growth  of  the  larvae. 
This  also  is  important,  since,  if  one  merely  gives  a  large  supply  of  food 
to  the  female  at  the  start  of  oviposition,  and  does  not  change  it,  the 
early-born  larvae  will  have  very  different  food  from  those  which  are 
born  later.    The  pupae  were  picked  out  of  the  "larval  dish"  and  placed 


INHERITANCE  OF  ABNORMAL  VENATION.  3 

upon  moist  blotting-paper  in  a  small  vial,  from  which  the  adults  could 
readily  be  transferred  to  an  etherizing  vial  as  they  emerged. 

When  mating  was  to  be  done  the  sexes  were  always  separated  before 
they  were  a  day  old.  Usually  no  female  was  used  as  a  parent  that  was 
more  than  12  hours  old  before  being  isolated  from  the  males.  Numer- 
ous tests  showed  that  no  females  so  treated  laid  fertile  eggs.  Only 
rarely  was  there  a  difference  of  more  than  one  day  in  the  ages  of  the 
parents,  and  they  were  usually  mated  before  they  were  two  days  old. 
For  practical  reasons,  parents  were  killed  after  50  to  100  offspring  had 
been  secured.  It  was  found  that  neither  the  percentage  of  abnormal 
offspring  nor  the  intensity  of  their  abnormalities  changed  with  the  age 
of  their  parents,  so  that  this  procedure  was  permissible. 

In  this  paper  only  those  families  are  considered  which  are  in  or  close 
to  the  main  line  of  descent.  I  have  not  thought  it  worth  while  to  include 
any  families  having  less  than  40  offspring  unless  they  were  in  this  main 
line.  Typical  data  are  given  in  table  36,  page  31.  I  have  tried  to  arrange 
these  so  that  they  will  be  available  for  further  work  by  those  interested. 
They  should  not,  however,  be  used  for  more  than  they  are  worth.  For 
example,  one  can  not  study  the  inheritance  of  fecundity  from  them,  as  in 
but  few  cases  have  I  bred  from  a  female  until  she  died  a  natural  death. 
All  individuals,  both  parents  and  offspring,  have  been  kept  for  refer- 
ence and  are  deposited  in  the  American  Museum  of  Natural  History. 
When  of  especial  interest,  the  wings  were  mounted  on  glass  slides  in  a 
thin  layer  of  paraffin.  This  was  found  to  be  an  excellent  method  of 
preservation.  By  all  other  methods  which  were  tried  the  veins  were 
rendered  more  or  less  transparent.  When,  as  in  making  matings,  it 
was  desired  to  examine  live  flies,  they  were  slightly  etherized.  They 
completely  revive  in  a  few  minutes.  All  examinations  for  abnormalities 
in  wing- venation  must  be  made  with  a  lens. 

Occasionally  the  larvae  were  attacked  by  a  disease  (?)  of  unknown 
origin  which  caused  them  to  crawl  out  of  the  food,  elongate,  and  die. 
When  this  disorder  appeared  in  a  dish  it  was  usually  fatal  to  all  the  larvae 
in  that  dish.  Otherwise,  Drosophila  bears  confinement  very  well.  Prac- 
tically all  the  larvae  which  hatch  complete  their  development.  My  ex- 
perience confirms  the  results  reached  by  Castle  (19066)  that  the  closest 
inbreeding  may  be  practiced  with  this  fly  for  generations  with  no  injuri- 
ous results.  Such  inbreeding  was  the  rule  in  this  work,  being  necessary 
in  long-continued  breeding  unless  unpedigreed  stock  be  used. 

DESCRIPTION  OF  NORMAL  VENATION. 

The  normal  venation  of  Drosophila  is  extremely  simple,  as  is  shown 
by  fig.  2.  The  costal  vein  reaches  to  the  fourth  of  the  five  longitudinal 
veins.  The  auxiliary  vein  is  incomplete  or  indistinct.  The  anal  cell  is 
present.  The  discal  and  second  basal  cells  are  united  and  the  first  pos- 
terior cell  is  not  appreciably  narrowed  in  the  margin. 


4  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

DESCRIPTION  OF  ABNORMAL  VENATION. 

It  is  probable  that  all  insects  occasionally  show  some  abnormality  of 
wing-venation.  In  my  experience  with  Drosophila  ampelophila  they 
occur  in  one-third  of  1  per  cent  of  wild  specimens.  The  data  concern- 
ing this  point  are  given  in  table  1.  In  these  the  abnormalities  consisted 
of  irregularities  of  the  second  longitudinal  vein  or  small  dashes  near  its 
distal  end  (similar  to  figs.  3  to  10).  Only  one  of  the  19  abnormal*  wild 
flies  I  have  seen  was  abnormal  in  both  wings. 

Table  1. — Percentage  of  wild  Drosophila  ampelophila 
which  have  extra  veins  in  their  wings. 


Normal. 

Abnor- 
mal. 

Percent- 
age of 
abnormal. 

Bloomsburg,  Pa 

Huntington,  N.  Y.  ... 
Woods  Hole,  Mass.... 
Boston,  Mass 

1165 

697 

2083 

1660 

8 

3 
3 
5 

0.68 
0.43 
0.14 
0.30 

Total 

5605 

19 

0.34 

While  rearing  this  insect  for  another  purpose,  several  such  abnormal 
specimens  were  found  in  one  family.  My  principal  abnormal  strain,  in 
which  the  variety  and  amount  of  abnormality  is  little  short  of  astound- 
ing, came  from  these.  The  various  figures  give  a  better  conception  of 
what  was  obtained  than  would  verbal  description.  There  is  the  utmost 
variation  in  the  abnormal  venation,  not  only  in  different  flies,  but  in  the 
different  wings  of  the  same  fly.  The  majority  of  the  abnormalities  are 
in  the  distal  portion  of  the  marginal  cell,  but  they  have  been  found  also 
in  the  submarginal  and  a  few  in  the  first,  second,  and  third  posterior 
cells,  affecting  all  the  longitudinal  veins  except  the  first. 

CORRELATION  BETWEEN  THE  RIGHT  AND  THE  LEFT  WINGS. 

One  wing  may  be  abnormal,  or  both  may  be.  In  the  latter  case  the 
abnormality  may  be  great  in  one  wing,  small  in  the  other ;  on  one  vein 
in  one  wing  and  lacking  on  this  vein  but  present  on  others  in  the  other 
.wing  (see  figs.  44  to  46).  Nevertheless  there  is  a  correlation  between 
the  intensity  of  the  abnormality  in  the  two  wings,  as  is  made  clear  by 
tables  2  and  3.  In  drawing  up  these  tables  the  range  of  variation  of 
the  intensity  of  the  abnormality  was  divided  arbitrarily,  since  the  char- 
acter is  not  quantitatively  measurable,  into  six  classes:  normal  vena- 
tion (or  zero  intensity  of  the  abnormality),  very  slight  (see  figs.  3  to  7), 
slight  (see  figs.  8  to  11),  medium  (see  figs.  12  to  18),  great  (see  figs. 
19  to  24),  and  very  great  (see  figs.  25  to  35).  To  which  class  a  given 
wing  should  be  assigned  is  a  matter  of  judgment ;  but  since  when  these 
tables  were  made  up  it  was  thought  that  there  was  no  correlation  be- 

*Unles3  otherwise  stated   "abnormal  venation"  means,    throughout  this    paper 
"veins  added."  &  F  F     ' 


INHERITANCE   OF  ABNORMAL   VENATION. 


tween  the  two  wings  with  respect  to  the  intensity  of  abnormality,  the 
personal  equation  which  entered  in  would  have  tended  to  make  the  cor- 
relation as  shown  by  the  tables  too  low  rather  than  too  high.    The  arabic 

Table  2. — Correlation  between  right  and  left  wings  of  males. 
[For  explanation  see  page  4.] 

RIGHT. 


N. 

V.  S. 

S. 

M. 

G. 

V.G. 

N. 

413 

340 

48 

79 

33 

46 

34 

58 

3 
17 

531 

V.  S. 

48 
60 

23 

12 

8 
8 

14 
10 

1 
3 

94 

S. 

23 

46 

15 
9 

9 

6 

15 
8 

9 

2 

71 

M. 

20 

47 

14 
10 

17 

7 

14 

8 

9 

2 

74 

G. 

3 
13 

3 
3 

2 

2 

9 

2 

2 

2 

1 

20 

V.  G. 

1 

1 

1 

507 

103 

69 

86 

25 

1 

791 

Table  3. — Correlation  between  right  and  left  wings  of  females. 
[For  explanation  see  page  4.] 

RIGHT. 


N. 

V.  S. 

S. 

M. 

G. 

V.G. 

N. 

226 
150 

43 
51 

37 

57 

47 
73 

1 
15 

5 

354 

V.  S. 

42 

46 

22 

16 

21 
27 

20 
25 

3 

6 

1 
2 

109 

s. 

25 

54 

20 

18 

33 
21 

37 
26 

12 
7 

1 

2 

128 

M. 

42 
67 

25 
23 

33 

25 

46 

10 

8 

2 

2 

158 

G. 

9 

21 

7 
7 

6 
8 

13 

20 

11 
5 

4 

1 

50 

V.G. 

6 

2 

2 

5 
3 

6 

4 

15 

344 

117 

130 

168 

43 

12 

814 

numbers  show  the  observed  conditions  ;  the  italics  show  the  distribution 
of  frequencies  which  would  have  been  expected  had  there  been  no  cor- 
relation. The  fact  that  expectation  is  exceeded  by  observation  in  those 
classes  where  the  intensity  is  alike,  or  nearly  so,  in  each  wing,  but  is  not 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


INHERITANCE  OF  ABNORMAL  VENATION. 


46  a 


8 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


equaled  in  the  classes  where  the  two  wings  markedly  differ,  indicates  a 
definite  positive  correlation. 

Furthermore,  when  one  wing  is  abnormal  the  chances  that  the  other 
one  will  be  abnormal  also  are  62  in  100  in  the  case  of  the  males  and  74 
in  100  in  the  case  of  the  females.  This  is  an  estimate  based  upon  4,000 
pedigreed  individuals.  It  will  probably  not  hold  for  wild  flies,  since  a 
large  part  of  the  4,000  were  from  the  abnormal  strain;  hence  the  esti- 
mated chances  are  larger  than  they  would  be  in  nature,  because,  as  will 
be  shown  shortly,  there  is  a  close  relation  between  the  percentage  of 
abnormal  offspring  in  a  family  and  the  likelihood  that  an  abnormal  fly 
will  be  abnormal  in  both  wings.  It  does,  however,  give  an  idea  of  the 
correlation  which  exists  between  the  two  wings  with  respect  to  the 
presence  or  absence  of  abnormal  venation  when  such  abnormalities  are 
well  fixed,  and  it  brings  out  the  further  point  that  there  is  a  sexual  dif- 
ference to  be  considered. 

SEXUAL    DIMORPHISM. 

The  females  show  a  greater  tendency  to  be  abnormal  than  do  the 
males,  and,  when  abnormal,  their  abnormalities  are,  on  the  average, 
more  intense  than  those  of  the  males.  The  first  of  these  points  is  illus- 
trated in  table  4  and  fig.  51.  Table  4  shows  the  percentage  of  abnor- 
mal males  and  females  in  200  families.  It  will  be  noted  that  as  the 
percentage  of  abnormal  males  increases  the  percentage  of  their  sisters 
which  are  abnormal  increases  until  the  latter  have  become  practically 
100  per  cent  abnormal.  Then,  since  they  can  go  no  further,  their 
brothers  gain  on  them  in  abnormality  until  we  get  families  in  which 
100  per  cent  of  both  males  and  females  are  abnormal.  In  fig.  51  the 
crosses  show  the  position  of  the  mean  percentage  of  abnormal  sisters  for 
each  10  per  cent  grade  of  abnormal  brothers.  A  line  is  drawn  to  show 
the  condition  when  for  each  per  cent  of  male  abnormality  the  female 
abnormality  is  1.5  per  cent.  Thus,  when  40  per  cent  of  the  males  are 
abnormal,  60  per  cent  of  their  sisters  are  abnormal.  Corresponding  to 
60  per  cent  male  abnormality,  we  get  90  per  cent  female  abnormality. 
Beyond  that  the  females  can  go  little  further,  hence  the  line  becomes 


INHERITANCE  OF  ABNORMAL  VENATION. 


TABLE  4. — Percentage  of  abnormal  males  and  females  in  200  families. 

Females 


.0 

5.0 

15.0 

25.0 

35.0 

4S.O 

55.0 

65.0 

75.0 

85.0 

95.0 

.0 

31 

II 

1 

43 

5.0 

2 

10 

7 

2 

21 

15.0 

1 

2 

3 

5 

1 

12 

25.0 

3 

2 

3 

4 

12 

350 

3 

3 

2 

3 

2 

1 

1 

15 

45.0 

3 

1 

3 

5 

'  12 

55.0 

A 

i 

3 

2 

10 

65.0 

1 

2 

l 

5 

9 

75.0 

1 

3 

6 

3 

f3 

8S.O 

3 

6 

9 

95.0 

l 

4-3 

44 

33 

22 

10 

8 

10 

7 

6 

12 

10 

17 

65 

200 

Females 


n 

n 

2 


0 

5 

15 

25 

35 

45 

55 

65 

75         85 

95 

o 

>%,■ + 

5 

15 

N.  + 

25 

s  + 

35 

\      + 

4-5 

+ 

55 

■KS. 

65 

4 

75 

+ 

85 

+ 

95 

+ 

Fig.  51.— For  explanation  see  p  8. 


10  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

vertical.    The  close  fit  of  this  line  to  the  observed  data  shows  that  the 
relation 

Percentage  of  abnormal  females  =  1.5  X  percentage  of  abnormal  males 

may  be  taken  as  approximately  describing  the  average  observed  con- 
dition. 

Owing  to  the  impossibility  of  describing  the  intensity  of  abnormality 
in  quantitative  grades,  we  can  not  give  a  formula  for  showing  its  sexual 
relation.  Tables  2  and  3  show  that  there  is  such  a  relation.  The  ques- 
tion as  to  whether  both  wings  or  only  one  shall  be  abnormal  is  also  a 
part  of  this  same  problem  of  the  variation  of  the  intensity  of  the  abnor- 
mality. We  have  seen  that  when  a  female  is  abnormal  she  will  in  74 
per  cent  of  the  cases  be  so  abnormal  that  both  wings  will  be  affected, 
while  only  62  per  cent  of  her  abnormal  brothers  will  be  abnormal  in  both 
wings. 

THE  RANGE  OF  VARIATION  OF  ABNORMALITY  INCLUDES  "NORMAL"  VENATION. 

One  other  point  is  to  be  noted.  The  intensity  of  abnormality  ranges 
all  the  way  from  cases  in  which  there  is  almost  as  much  abnormal  vena- 
tion as  normal  down  to  a  barely  discernible  devia- 

Table  5 
tion  from  normality.     We  have,  then,  in  studying 

the  inheritance  of  abnormal  venation,  the  serious 
difficulty  that  a  just  indiscernible  abnormality  may 
be  present.*  Such  a  fly  would  be  recorded  as  nor- 
mal. Table  5  suggests  that  they  would  be  more  like- 
ly to  occur  in  families  in  which  the  percentage  of 
abnormal  offspring  is  low,  for  as  such  percentage 
decreases  the  percentage  of  abnormal  individuals 
which  are  abnormal  on  both  sides  (C.  S. )  decreases.  In  other  words, 
there  is  an  increasing  percentage  of  abnormal  flies  which  have  the  abnor- 
mality so  reduced  that  in  at  least  one  wing  it  can  not  be  seen.  Hence, 
presumably,  there  is  an  increasing  percentage  of  flies  which  have  the 
abnormality  reduced  in  both  wings  to  a  point  just  below  visibility. 
These  will  be  more  common  among  males  than  among  females,  because 
the  intensity  of  the  abnormality  is  less  in  male  than  in  female  wings. 
Whether  this  alone  accounts  for  the  fact  that  a  smaller  percentage  of 
brothers  are  visibly  abnormal  than  of  sisters  is  a  question  to  which  it  is 
difficult  to  give  an  answer. 

•  *M^l  ^°i  this  be  true  aIso  of  the  sP°tted  condition  in  certain  mammals?  A  guinea- 
pig  still  behaves  as  a  spotted  animal  even  if  the  spots  are  reduced  until  only  the  eyes 
remain  affected.  If  the  variation  goes  still  further  we  would  have  an  animal  germi- 
"  1  t  S^°"te     somatlcally  sPotless-     We  would  then  say  that  the  spotted  condition  is 


|  Percentage  of 

•  abnormal  flies 

C.  s. 

per  family. 

lto   20... 

20.9 

21  to   40... 

30.9 

41  to   60... 

50.6 

61  to   80... 

58.0 

81  to  100... 

83.1 

INHERITANCE  OF  ABNORMAL  VENATION.  11 

HISTORY  OF  THE  PEDIGREED  STRAIN. 

Before  taking  up  the  data  concerning  inheritance,  it  will  be  well  to  out- 
line briefly  the  history  of  the  chief  pedigreed  strains.  Further  details 
are  given  in  table  36.  Mating  211  was  the  first  family  in  these  lines  of 
which  a  large  number  of  offspring  were  described.  Both  parents  were 
abnormal  in  both  wings.  The  wings  of  177  offspring  of  this  mating  were 
sketched.  It  was  found  that  31  per  cent  of  the  males  were  abnormal 
and  65  per  cent  of  the  females.  Successive  generations  after  this, 
breeding  brother  with  sister,  gave  the  following  results:  Abnormal 
female  by  normal  male  (mating  257) ,  70  per  cent  of  each  sex  abnor- 
mal; abnormal  female  by  abnormal  male  (mating  284),  62  per  cent  of 
the  males  and  96  per  cent  of  the  females  abnormal;  abnormal  female 
by  normal  male  (mating  330),  96  per  cent  of  the  males  and  91  per 
cent  of  the  females  abnormal;  abnormal  female  by  normal  male  (mat- 
ing 367) ,  64  per  cent  of  the  males  and  91  per  cent  of  the  females  abnor- 
mal. A  number  of  matings  were  made  from  the  offspring  of  No.  367. 
Matings  405  and  408  are  of  especial  interest. 

In  both  of  these  matings  both  parents  were  abnormal  in  both  wings. 
Unfortunately  there  were  a  small  number  of  offspring  from  each  (25 
and  29,  respectively),  but  all  of  the  offspring  of  mating  405  were  normal 
and  all  those  of  mating  408  were  abnormal.  Three  matings  were  made 
from  the  offspring  of  405.  Of  the  385  offspring  of  these,  not  a  single 
one  showed  the  slightest  trace  of  an  abnormality,  while  of  the  51 
offspring  of  mating  440  (the  parents  being  children  of  408)  only  one,  a 
male,  was  free  from  abnormal  venation.  Mating  405,  then,  became  the 
starting-point  of  the  "normal  strain"  and  mating  408  the  starting-point 
of  the  "abnormal  strain." 

As  can  be  seen  from  table  36,  the  various  generations  of  the  abnormal 
strain  gave  approximately,  sometimes  actually,  100  per  cent  abnormal 
flies,  although  normal  individuals  were  far  from  rare.  Furthermore, 
the  intensity  of  the  abnormalities  increased.  The  greatest  abnormality 
noticed  before  the  fifth  generation  is  shown  in  fig.  20.  Up  to  that  time 
all  abnormalities  were  confined  to  the  second  longitudinal  vein.  Begin- 
ning with  the  sixth  generation,  abnormalities  appeared  on  the  third 
longitudinal  vein.  They  became  frequent  by  the  tenth  generation.  In 
the  fifteenth  generation  they  were  common  and  abnormalities  began  to 
be  noticed  on  the  fourth  longitudinal  vein.  These  have,  even  yet,  rarely 
exceeded  small  spurs  near  the  distal  end.  About  this  time  the  fifth 
longitudinal  vein  also  began  to  be  affected,  and  specimens  such  as  are 
illustrated  in  figs.  30  and  32  were  found.  Meanwhile  increasingly  great 
abnormalities  on  the  second  and  third  longitudinal  veins  occurred.  (See 
figs.  37  to  42  for  examples.     The  condition  shown  in  fig.  43  is  unique. ) 

Turning  now  to  the  normal  strain,  three  points  should  be  borne  in  mind : 
the  parents  in  each  generation  were  normal,  it  came  from  the  same 


12 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


ancestry  as  the  abnormal  strain,  and  about  one- third  of  1  per  cent  of 
wild  Drosophila  ampelophila  were  found  to  be  abnormal.  For  four 
generations  after  branching  from  the  abnormal  strain  (five,  counting 
mating  405)  not  a  single  abnormal  individual  was  found,  but  in  the  next 
generation  1  fly  out  of  216  (0.5  per  cent)  had  a  very  slight  abnormality. 
In  succeeding  generations  the  percentage  increased  for  a  time,  in  spite 
of  artificial  selection  to  the  contrary,  and  then  diminished  to  zero  under 
the  same  treatment.  The  abnormalities  were  all  small,  never  greater 
than  "medium."  Table  6  summarizes  the  history  of  this  strain  for  40 
generations. 

Table  6. — Fluctuation  in  percentage  of  abnormal  individuals  in  a  normal  strain. 


Generations 

of  normal 

strain. 


No.  of 
normal. 


1  and  2 
3  4 


5 
7 
9 
11 
13 
15 
17 
19 
21 


6 

8 

10 
12 
14 
16 
18 
20 
22 


418 
235 
575 
594 
336 
471 
183 

79 
110 
234 

56 


No.  of 

Percentage  ! 

of 
abnormal. 

abnormal. 

0 

0.0 

0 

0.0 

1 

0.2 

7 

1.2 

31 

8.4 

45 

8.7 

14 

7.1 

2 

2.5 

5 

4.3 

14 

5.6 

2 

3.4 

Generations 

of  normal 

strain. 


23  and  24 


25 
27 
29 
31 
33 
35 
37 
39 


26 
28 
30 
32 
34 
36 
38 
40 

Total 


No  of 

No.  of 

Percentage 

of 
abnormal. 

normal. 

abnormal. 

144 

0 

0.0 

239 

0 

0.0 

257 

1 

0.4 

116 

0 

0.0 

195 

0 

0.0 

217 

0 

0.0 

148 

0 

0.0 

55 

0 

0.0 

63 

0 

0.0 

4,725 

122 

2.5 

It  is  to  be  noted  that  the  percentage  of  abnormal  individuals  is  greater 
in  this  strain  artificially  selected  for  normal  venation  than  it  is  in  nature. 
At  first  thought  one  would  say  that  this  is  an  effect  of  the  environment 
to  which  they  were  subjected.  If  this  be  true,  environment  may  have 
played  a  part  in  the  production  of  the  abnormal  strains.  I  think,  how- 
ever, that  it  is  not  true.  A  sufficient  explanation  seems  to  lie  in  the 
fact  that  a  form  of  selection  exists  in  nature  which  is  keener  than  the 
artificial  sort,  even  when  the  latter  is  carried  out  under  a  lens. 

THE  EEFECT  OF  SELECTION. 

Of  late  years  there  has  arisen  considerable  skepticism  concerning  the 
cumulative  effect  of  selection  except  as  a  means  of  isolating  "pure 
lines."  Jennings  (1908)  says  :  "Certainly,  therefore,  until  some  one 
can  show  that  selection  is  effective  within  pure  lines,  it  is  only  a  state- 
ment of  fact  to  say  that  all  experimental  evidence  is  against  this." 
Whether  or  not  the  present  material  has  a  bearing  upon  the  question 
thus  clearly  put  depends  upon  the  definition  of  a  pure  line.  If  a  pure 
line  be  defined  as  one  from  which  nothing  else  can  be  gotten  by  selec- 
tion, further  discussion  is  not  necessary.  On  the  other  hand,  if  inbreed- 
ing (for  the  most  part,  brother  X  sister)  for  10  or  15  generations  and 
rigid  selection  (in  this  case,  with  respect  to  wing-venation)  may  be 


INHERITANCE  OF  ABNORMAL  VENATION.  13 

reasonably  supposed  to  have  established  as  "  pure  "  a  line  as  exists  in  a 
given  case,  the  following  facts  may  be  of  interest. 

The  abnormalities  obtained,  both  in  the  direction  of  veins  added  and 
of  veins  lacking,  far  surpass  those  found  in  nature  in  this  or  any  other 
insect  with  which  I  am  familiar.  Furthermore,  they  do  not  even  remotely 
suggest  the  venation  of  any  of  this  fly's  relatives.  Something  new  has 
been  produced.  In  the  strain  whose  early  history  has  just  been  described 
there  was,  at  the  start,  no  definite  effort  made  to  build  up  an  abnormal 
race  as  quickly  as  possible.  Later  I  tried  to  do  this  from  wild  material 
obtained  from  other  localities. 

Starting  with  an  abnormal  male  and  a  normal  female  from  Boston  and 
an  abnormal  male  and  female  from  Bloomsburg,  Pennsylvania,  I  rigidly 
selected  for  additional  veins.  The  record  for  each  successive  set  of  two 
generations  was  8.8,  5.5,  11.5,  14.3,  30.3,  45.8,  85.9,  and  100  per  cent 
abnormal.  Thereafter  mass-breeding  was  practiced  and  the  abnormal 
strain  preserved  for  about  a  year  by  merely  starting  a  fresh  jar  every 
couple  of  weeks  with  the  most  abnormal  individuals  found  at  that  time. 

The  abnormalities  in  this  strain  were  of  the  same  nature  and  extent 
as  in  the  one  started  from  the  Long  Island  material.  It  would  seem 
that  this  increase  in  the  percentage  of  abnormal  individuals  up  to  100 
per  cent  and  the  subsequent  increase  of  the  intensity  of  the  abnormalities 
can  not  be  due  to  the  gradual  weeding  out  of  all  units  but  the  one  or 
several  desired,  because  one  quickly  gets  things  which  one  can  safely 
say  did  not  exist  in  the  population  with  which  we  started,  or,  to  be  more 
exact,  which  we  do  not  see.  Some  can  probably  imagine  that  the  '  units" 
for  each  successive  grade  of  abnormality  existed  in  the  parents  with 
which  we  started,  but  that  they  were  held  in  check  by  an  equal  number 
of  inhibiting  "units  "  of  corresponding  powers,  so  that  the  result  could 
be  explained  by  saying  that  in  the  selection  we  cut  out  step  by  step  suc- 
cessively stronger  inhibiting  units,  thus  allowing  successively  greater 
abnormality-producing  units  to  manifest  themselves.  On  any  other 
hypothesis,  it  seems  to  me,  we  must  admit  the  cumulative  effect  of 
selection  upon  a  "unit,"  i.  e.,  within  a  pure  line. 

But,  upon  this  hypothesis,  how  can  we  account  for  the  occasional  nor- 
mal flies?  Why  do  not  the  inhibiting  units  stay  cut  out  after  we  have 
once  gotten  rid  of  them  so  thoroughly  that  all  the  flies  of  several  suc- 
cessive generations  show  strong  added  veins?  Perhaps  they  do  stay 
cut  out  and  these  occasional  normals  are  merely  fluctuating  variations 
in  the  abnormal  unit.  If  so,  and  if  selection  does  not  have  a  cumula- 
tive effect  within  a  unit,  it  would  be  impossible  to  return  to  normality 
from  a  series  of  inbred  generations  of  abnormality.  But  it  is  possible. 
Starting  with  a  family  which  had  one  normal  offspring  in  a  total  of  133 
(99.2  per  cent  abnormal)  and  selecting  to  reduce  the  extra  veins,  the 
percentage  of  abnormal  offspring  in  successive  generations  was  81.8, 
66.2,  32.9,  12.5,  17.0,  0.0,  0.0,  0.0,  and  so  on,  as  a  typical  normal  strain. 


14  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

The  building  up  of  an  abnormal  strain  from  a  long-inbred  normal  one 
was  also  nearly  completed  when  it  was  stopped  by  accident.  I  did  not 
think  it  worth  while  to  start  it  anew,  as  its  accomplishment  would  prove 
little,  since  it  might  be  said  that  the  normal  strain  was  a  "mixed  general 
population"  due  to  normality  (inhibiting)  units  masking  all  sorts  of 
latent  abnormality  units. 

In  nature  a  small  percentage  of  flies  have  the  fifth  longitudinal  vein 
somewhat  shortened  (see  fig.  47) .  This  variation  also  appears  in  the 
experimental  strains.  Rather  as  a  matter  of  curiosity,  I  selected  for 
shortened  veins  during  a  few  generations  and  very  quickly  obtained  such 
specimens  as  are  illustrated  in  figs.  48  to  50.  One  can  not  go  further 
in  this  direction  without  some  special  technique,  because  the  wings, 
lacking  the  support  of  the  veins,  droop  and  catch  in  the  fly's  food. 
Probably  breeding  could  be  continued  by  cutting  off  the  parent  wings 
when  matings  are  made.  I  did  not  try  it,  as  it  was  already  very  evident 
that  selection  was  just  as  effective  in  the  negative  as  in  the  positive 
direction. 

On  the  other  hand,  all  attempts  to  fix,  by  selection,  some  particular 
type  of  abnormality  utterly  failed.  It  was  thought  possible  that  the 
great  variety  of  forms  which  the  extra  veins  showed  was  due  to  a  mix- 
ture of  a  number  of  simple  forms  and  that  selection  might  isolate  these 
simple  types.  The  most  hopeful  was  a  simple  forking  of  the  second 
longitudinal  vein  (see  fig.  10) .  Selection  for  this  type  was  started  sev- 
eral times,  but  never  went  beyond  the  fifth  generation,  because,  although 
there  were  plenty  of  abnormal  flies  in  each  generation,  there  was  no 
increase  in  the  number  showing  this  particular  type,  and  sooner  or  later 
a  generation  would  contain  none  of  them  from  which  to  breed.  The 
same  was  true  in  the  experiments  aimed  to  fix  the  abnormality  on,  for 
example,  the  third  longitudinal  vein,  but  to  keep  it  off  of  the  second. 
It  is  easy  to  have  all  the  abnormal  flies  abnormal  only  on  the  second 
longitudinal  vein,  providing  one  be  content  with  small  abnormalities. 
However,  as  soon  as  one  increases  greatly,  by  selection,  the  abnormality 
on  the  second  vein,  the  other  veins  begin  to  be  abnormal. 

These  are  the  facts:  Starting  with  slight  extra  veins,  either  in  wild 
material  or  in  material  selected  and  inbred  for  normal  venation,  we 
can  quickly  get  by  selection  100  per  cent  abnormal  offspring.  In  future 
generations  this  strain  can  be  quickly  brought  back  again  to  its  normal 
condition  by  selection.  Selection  also  quickly  shortens  the  veins  and 
would  probably  largely  do  away  with  them,  provided  some  technique 
were  adopted  to  keep  the  results  of  selection  alive.  But  selection, 
accompanied  by  the  strictest  inbreeding  (brother  X  sister  and  parent  X 
child)  failed  to  isolate  any  unit  characterized  by  a  given  form  or  extent 
of  abnormality. 

The  interpretation  of  these  facts  would  doubtless  vary  with  varying 
opinions  as  to  unit-characters. 


INHERITANCE  OF  ABNORMAL  VENATION. 


15 


THE  DATA  CONCERNING  INHERITANCE. 

Without  reference  to  the  grandparents,  the  data  are  summarized  in 
table  7: 

Table  7. 


Crosses. 

Average 

p.  ct,  of 

abnormal 

offspring. 

Normal  X  normal 

9.6 
35.8 
54.7 
85.9 

Abnormal  male  X  normal  female... 
Normal  male  X  abnormal  female... 
Abnormal  X  abnormal 

In  this  work  a  fly  is  counted  as  abnormal  if  there  is  the  slightest  trace 
of  abnormality  in  either  wing.  These  results  leave  no  room  for  doubt 
concerning  the  heritability  of  the  tendency  toward  extra  veins. 

Tables  8  to  19  show  the  relation  between  various  ancestors  and  the 
offspring.  The  coefficients  of  association  found  from  these  are  given 
below  the  respective  tables.  Although  these  coefficients  are  greater 
than  expectation  on  the  basis  of  Pearson's  Law  of  Ancestral  Heredity, 
they  do  not  negative  his  conclusions.  He  was  very  careful  to  exclude 
cases  in  which  there  is  inbreeding  or  assortative  mating.  Both  were 
largely  practiced  in  these  experiments.  These  coefficients  do  show,  how- 
ever, that  change  of  sex  in  the  ancestry  does  not  uniformly  weaken  in- 
heritance. Thus,  the  average  coefficient  of  association  between  father 
and  sons,  and  mothers  and  daughters  (no  change  of  sex)  is  0.78 ;  and 
that  between  father  and  daughters,  mothers  and  sons  (one  change  of 


Table  8. 

SONS. 


Table  9. 

DAUGHTERS. 


N. 

A. 

<& 

H 

B 

< 

N. 

A. 

N. 

2949 

837 

3786 

N. 

3011 

13-20 

4340 

A. 

1241 

1948 

3189 

A. 

951 

2703 

3714 

4190 

2785 

6975 

3962 

4092 

8054 

C.  A.=0.694. 


C.  A.  =0.736. 


Table  10. 

SONS. 


Table  11. 

DAUGHTERS. 


N. 

A. 

H 

3 

o 

N. 

A. 

N. 

2801 

465 

3266 

N. 

2^83 

746 

8729 

A. 

1389 

2320 

3709 

A. 

979 

3346 

43-:.-) 

4190 

2785 

6975 

3962 

4092 

8054 

C.  A.  =0.819. 


C.  A.  =0.864 


16 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


2fc 


Table  12. 

SONS. 


N. 

A. 

N. 

2813 

1079 

2892 

A. 

1329 

1705 

3034 

4142 

2784 

6926 

B  Eh 


Table  13. 

DAUGHTERS. 


N. 

A. 

N. 

2602 

1855 

4457 

A. 

1310 

2228 

3538 

3912 

4083 

7995 

C.  A.  =0.540. 


C.  A.=0.409. 


2  ta 
6,  «=• 


Table  14. 


SONS. 


N. 

A. 

N. 

2535 

4b4 

3019 

A. 

1607 

2300 

3907 

4142 

2784 

6926 

C.  A.  =0.765. 


Table  15. 

DAUGHTERS. 


N. 

A. 

N. 

2727 

759 

3486 

A. 

1185 

3324 

4509 

3912 

4083 

7995 

C.  A.  =0.820. 


-2d 

S3 


Table  16. 

SONS. 


N. 

A. 

N. 

2766 

1015 

3781 

A. 

1339 

1761 

3100 

4105 

2776 

6881 

£« 


Table  17. 

DAUGHTERS. 


N. 

A. 

N. 

2619 

1768 

4387 

A. 

1262 

2296 

3558 

3881 

4064 

7945 

C.  A.  =0.672. 


C.  A.  =0.459. 


Table  18. 

SONS. 


N. 

A. 

N. 

2444 

•477 

2921 

A. 

1661 

2299 

3960 

4105 

2776 

6881 

C.  A.  =0.753. 


-    — 

aB 


Table  19. 

DAUGHTERS. 


N. 

A. 

N. 

2630 

741 

3371 

A. 

1251 

3323 

4574 

3881 

4064 

7945 

C.  A.  =0.808. 


sex)  is  also  0.78.  Considering  the  grandparents,  the  average  coefficient 
of  association  between  sons  and  father's  father,  and  daughters  and  the 
mother's  mother  (no  change  of  sex)  is  0.67,  while  that  between  sons 
and  the  mother's  father,  and  daughters  and  the  father's  mother  (two 
changes  of  sex)  is  0.74.  This  result  agrees  with  that  of  Blanchard 
(1903)  concerning  the  coat-color  of  horses  and  is  not  in  harmony  with 
Pearson's  (1900)  and  the  writer's  (1903)  concerning  the  eye-color  in  man. 


North  Carolina  State  Library 

INHERITANCE  OF  ABNORMAuVftlK^ON. 


17 


Table  20. — Relation  between  degree  of 
abnormality  in  parents  and  percent- 
age of  abnormal  offspring. 


It  will  be  convenient  in  the  present  discussion  to  adopt  the  following 
symbols:  Ai  denotes  a  fly  that  is  abnormal  in  one  wing  only;  A_>,  a  fly 
abnormal  in  both  wings,  and  C.  S. 
(coefficient  of  symmetry)  that  per- 
centage of  a  given  lot  of  abnormal 
flies  which  are  abnormal  in  both 
wings.  Tables  20  and  21  may  be 
summarized  as  follows:  Flies  which 
are  so  abnormal  that  both  wings  are 
affected  not  only  gave,  on  the  aver- 
age, a  greater  percentage  of  abnor- 
mal offspring  than  flies  abnormal  in 

only  one  wing,  but  the  abnormal  offspring  of  the  former  were  more 
likely  to  be  abnormal  in  both  wings  than  those  of  the  latter.     It  must 

Table  21. — Relation  between  parents  and  offspring  with  respect  to  one  wing  or  both 

being  abnormal. 


Parents 

p.  ct  of 
abnormal 
offspring. 

Parents. 

A-2  X   -**-2 

i  Ajx  A, 

85.1 
76.8 
71.9 

NX  A., 
NX  A, 
N  X  N 

P.  <  t.  of 
abnormal 
oflbpring. 

45.8 
351 
138 


Parents. 

Offspring. 

Parents. 

Offspring. 

Male. 

Female. 

A, 

A* 

C.  s. 

Male. 

Female. 

A, 

A2 

A2 
A2 
A2 
A, 
A, 

A2 

A: 

N 

A2 

A, 

268 
102 
105 
149 
83 

1271 

178 
118 
428 
158 

0.83 
0.64 
0.52 
0.74 
0.66 

A, 

N 
N 
N 

N 

A2 

A, 

N 

55 

122 
57 

285 

61 

198 

53 

160 

0.53 
0.62 
0.48 
0.36 

Table  22.—  Relation  between  parents  and 
offspring  with  respect  to  ichich  wing 
is  abnormal. 

[AR=Abnormal  in  right  wing  only;  -V  Abnor- 
mal in  left  wing  only;  \.:  Abnormal  in 
both  wings;  Aj  =  Abnormal  in  one  wins 
only.] 


be  noted  that  this  was  only  "on  the  average."  Although  it  was  an 
exceptional  case,  we  have  seen  that  all  the  offspring  of  mating  405 
were  normal.  The  parents  each  had 
"great"  abnormality  in  both  wings. 

From  table  22  it  seems  evident 
that  a  given  asymmetry  (abnormal 
in  the  right  wing  only  or  abnormal 
in  the  left  wing  only)  is  not  inher- 
ited. The  offspring  of  a  parent 
which  is  abnormal  in  the  left  wing 
only  are  as  likely  to  be  abnormal  in 
the  right  as  in  the  left  wing,  and 
vice  versa.  This  is  in  accord  with  the 
results  obtained  by  Castle  (1906a) 
for  polydactylism  of  guinea-pigs, 
Larrabee  (1906)  for  the  reversed 
optic  chiasma  of  fishes,  and  Priz- 
bram  (1907)  for  eye-color  of  cats. 

As  was  pointed  out,  all  attempts 
to  fix  any  particular  form  of  abnor- 
mality  by  selection  and  inbreeding  (pure  lines?)  have  failed  ;   nor  has 


1 

Parents. 

Offspring. 

AR 

A, 

A, 

A2  X  A2 

147 

121 

+0.10 

A.2  X  An 

58 

79 

-0.15 

A2X  AL 

56 

58 

-0.02 

36 

41 

—0-06 

30 

25 

+0.09 

A.X  A, 

23 

24 

-0.02 

NXA, 

29 

18 

+0.23 

N  x  A, 

37 

28 

+0.14 

N  XN 

146 

139 

+0.02 

N  XA, 

121 

106 

+0."7 

18  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

there  been  any  apparent  tendency  to  settle  down  to  any  definite  type.  * 
The  "center  of  disturbance  "  has  remained  in  the  distal  portion  of  the 
marginal  cell  closely  related  to  the  second  longitudinal  vein.  Next  to 
the  second,  the  third  vein  has  been  the  most  affected,  then  the  fifth; 
but  I  have  failed  to  fix  the  abnormalities  in  these  veins.  They  are, 
apparently,  all  the  effects  of  the  disturbing  factor  or  factors,  centered 
on  the  second  longitudinal  vein  in  the  marginal  cell. 

The  hundreds  of  families  studied  showed  that  it  is  impossible  to  pre- 
dict, from  the  character  of  the  ancestors,  what  the  form  of  the  abnor- 
mality will  be  in  the  offspring.  The  most  that  one  can  do  is  to  give  an 
approximate  estimate  of  the  percentage  of  abnormal  individuals  and  a 
still  less  exact  prediction  of  the  average  intensity  of  the  abnormalities. 

THE  BEARING  OF  THESE  DATA  UPON  PROPOSED  LAWS  OF  HEREDITY. 

In  my  former  paper  (1907)  I  considered  that  normal  venation  is  more 
or  less  dominant  over  abnormal  in  the  Mendelian  sense.  Such  was  the 
case  in  the  early  part  of  the  work,  although,  as  was  pointed  out,  it  was 
the  spirit  only  and  not  the  letter  of  the  law  which  was  followed.  When 
a  normal  fly,  having  normal  ancestors,  was  crossed  with  an  abnormal 
one,  practically  all  the  offspring  were  normal.  The  abnormalities  which 
did  appear  were  slight,  but  there  was  no  doubt  about  their  presence. 
Matings  318  to  322  (see  table  36)  illustrate  such  cases.  The  offspring 
of  matings  347  to  353  are  second-generation  hybrids  from  such  a  cross. 
They  show  a  condition  not  very  divergent  from  the  Mendelian  expecta- 
tion. 

Since  the  number  of  offspring  in  most  of  the  families  considered  here 
is  large,  the  Galtonian  formula  can  be  tested  in  single  families,  and  it  is 
evidently  not  at  all  in  accord  with  the  data.  Neither  is  Pearson's  modi- 
fication of  it.  The  fact  that  normal  X  abnormal  gave,  in  large  families, 
practically  all  normal  completely  negatives  for  these  data  all  theories 
which  are  founded  on  the  hypothesis  of  equipotency  of  the  two  parental 
characters. 

On  the  other  hand,  while  the  results  of  certain  matings  accord  with 
Mendelian  expectation,  the  fit  is  far  from  good  in  the  majority  even  in 
the  early  generations.  For  instance,  we  have  seen  that  neither  normal 
nor  abnormal  breeds  true.  A  Mendelian  recessive  would  be  expected  to 
do  so  ;  therefore  we  can  not  consider  either  normality  or  abnormality 
to  be  Mendelian  unit-characters  in  that  sense. 


*Here  again  (see  p.  10)  the  similarity  to  the  experience  of  breeders  of  spotted  ani- 
mals is  interesting.  Castle  (1905),  for  example,  found  that  "one  can  by  selection 
progress  in  either  direction  through  this  series  of  changes,  either  increasing  or  de- 
creasing the  number  and  extent  of  the  pigment  patches,  but  it  is  impossible  without 
long-continued  selection  to  fix  the  color-pattern  at  any  particular  stage  in  the  series; 
perhaps  it  is  wholly  impossible  to  do  so,  as  Cuenot  (1904)  asserts  on  the  basis  of  his 
studies  on  mice,  but  this  I  very  much  doubt." 


INHERITANCE   OF  ABNORMAL  VENATION. 


19 


Fig.  52  shows  graphically  the  results  of  the  three  sorts  of  matings  : 
normal  X  normal,  normal  X  abnormal,  and  abnormal  X  abnormal.  The 
first  should  give  one  mode  at  zero  abnormality  and  another  at  25  per 
cent  abnormality  on  the  assumption  that  normality  is  dominant  in  the 
sense  in  which  the  term  is  now  used  in  Mendelian  literature.  These 
modes  would  represent  the  results  of  DD  X  DD  and  DR  X  DR,  respec- 
tively. They  are  present,  but  the  curve  runs  all  the  way  up  to  65  per 
cent  abnormal.  The  second  should  give  one  mode  at  zero  and  another 
at  50  per  cent,  representing  the  results  of  DD  X  RR  and  DR  X  RR,  respec- 
tively.    The  mode  at  5  per  cent  is  marked  and  might  be  explained  as  the 


48 
46 
44 
42 
40 
38 
36 
34 
32 
30 


■  Normal  x  Normal 
•Normal  x  Abnormal 
•Abnormal  x  Abnormal 


0  5  15  25  35         45  55  65  75         65         95 

Percentage    of    abnormal    individuals 
Pig.  52. 

result  of  "incomplete  dominance, "  a  thing  which  is  itself  badly  in  need 
of  a  Mendelian  explanation.  At  50  per  cent  there  is  a  drop  in  the  curve 
where  there  should  be  a  mode.  There  is  a  strong  mode  at  75  per  cent, 
where  there  should  be  none.  This  is  true  both  when  the  male  is  the 
normal  parent  and  when  the  male  is  the  abnormal  one  (see  fig.  53). 
Abnormal  X  abnormal  should  have  but  a  single  mode,  100  per  cent  (or 
95  per  cent  as  the  figure  is  drawn), representing  the  result  of  RR  <  RR. 
Such  a  mode  is  pronounced  in  the  curve,  being  chiefly  made  up  of  the 
families  of  the  abnormal  strain  after  generation  vn,  but  the  curve 
reaches  all  the  way  to  zero. 

These  data  are  analyzed  in  tables  24  to  35,  so  that  there  is  no  need  of 
a  further  text  description  of  them.   They  are  taken  from  the  early  part 


20  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

of  the  work.     The  results  of  the  seven  crosses  between  the  abnormal 

and  normal  strains  in  the  fifty-ninth  generation— all  that  were  made  at 

that  time— are  of  interest  in  this  connection  and  are  shown  in  table  23. 

Any  theory  applied  to  these  data  must  accord  with  the  following  facts: 

(1)  Abnormalities  occasionally  appear  in  the  venation  of  the  wings 
of  wild  Drosophila  ampelophila.  These  are  usually  added  veins.  Since 
evolution  in  the  Diptera  has  been  accompanied  by  a  reduction  in  the 
number  of  veins,  these  abnormalties  are  of  the  nature  of  "reversions. " 
The  tendency  to  produce  extra  veins  is  inherited  and  has  been  increased 
by  selection.     This  is  also  true  of  the  tendency  to  shortening  of  veins. 

n  9  /\      Male  abnormal  x  Female   normal 

5>  s         .  \     Male  normal  x  Female  abnormal 

1'    '  \ 

° A       A     \  ,         \  -'     /      ^ 

1 2  /     \  ><  >^"*      '        V 

§    I  •/  V  % -K  -« *  N 

2    i — ■ *» 

O  5  15         25         35        45         55         65         75         85         95 

Percentage   of    abnormal    individuals 
Fig.  63. 

An  examination  of  more  than  50,000  abnormal  wings  has  revealed  an 
immense  diversity  of  forms  which  the  abnormality  assumes.  Not  only 
are  new  forms  being  constantly  discovered,  but  the  intensity  of  the  ab- 
normality has  constantly  increased  as  long  as  selection  for  that  end  has 
been  kept  up.  The  limit  of  the  increase  was  apparently  not  reached,  but 
the  extra  veins  have  always  been  very  crude,  only  rarely  assuming  a 
form  and  position  comparable  to  ordinary  veins. 

(2)  A  greater  percentage  of  females  than  of  males  is  abnormal.  The 
formula 

Percentage  of  abnormal  sisters  =  1.5  X  percentage  of  abnormal  brothers 

approximately  describes  the  average  condition  in  the  various  families. 
Attempts  to  change  significantly  this  relation  have  failed,  and  seem 
destined  to  fail,  for  change  of  sex  in  the  ancestry  does  not  weaken 
inheritance. 

(3)  The  lower  range  in  the  variation  of  abnormality  certainly  includes 
barely  discernible  deviations  from  normality  and  presumably  just  indis- 
cernible deviations  also.     The  latter  would  be  considered  normal. 

(4)  Frequently  one  wing  of  a  fly  is  abnormal,  the  other  not  visibly  so. 
There  is  a  direct  relation  between  the  percentage  of  abnormal  offspring 
of  a  given  mating  which  are  abnormal  in  both  wings  and  the  total  per- 
centage of  abnormal  offspring.  Furthermore,  on  the  average,  parents 
which  are  abnormal  in  both  wings  give  a  larger  percentage  of  abnormal 


INHERITANCE  OF  ABNORMAL  VENATION.  21 

offspring  than  those  which  are  abnormal  in  one  wing  only.  There  is  no 
relation  between  parents  and  offspring  with  respect  to  the  side  upon 
which  asymmetrical  abnormalities  occur.  There  is  a  correlation  between 
the  two  wings  of  individual  flies  with  respect  to  the  intensity  of  the 
abnormality. 

(5)  Normal  male  X  abnormal  female  gives  a  greater  percentage  of 
abnormal  offspring  than  the  reciprocal  cross. 

(6)  Not  only  has  the  abnormality  increased  in  the  abnormal  strain, 
but,  in  spite  of  artificial  selection  to  the  contrary,  an  increasingly  large 
number  of  abnormal  individuals  appeared  for  a  while  in  the  normal  strain 
and  then  with  the  same  treatment  the  percentage  again  decreased. 
When  the  flies  are  allowed  to  choose  their  own  mates  the  percentage  of 
abnormals  is  kept  low  even  when  abnormal  flies  are  added  from  time 
to  time. 

(7)  Abnormality  originally  behaved  somewhat  like  a  Mendelian  reces- 
sive, but  in  the  later  generations  departed,  in  its  behavior,  very  far 
from  that  theory  as  it  is  now  understood. 

There  would  be  little  profit  in  reviewing  the  various  modifications  of 
the  simple  Mendelian  formula  and  pointing  out  in  detail  why  they  are 
not  satisfactory  in  the  present  case.  I  have  tried  most,  if  not  all,  of 
those  which  have  been  proposed  and  also  a  number  of  original  hypothe- 
ses involving  two  or  more  allelomorphs.  All  these  attempts  have  been 
failures  with  the  exception  of  the  idea  of  variation  of  potency  (Lutz, 
1907).  If  sufficiently  elaborated  this  will  "explain"  each  of  the  con- 
ditions set  forth  above,  and  until  quite  recently  I  believed  that  the 
inheritance  of  the  abnormal  venation  followed  this  modification  of  the 
Mendelian  law.  It  seemed  quite  probable  that  there  was  a  single  pair 
of  allelomorphs  involved — the  abnormality-producing  factor  and  its  ab- 
sence —  but  that  the  strength  of  the  positive  one  varied,  and  that  these 
variations  were  inherited,  making  the  problem  a  combination  of  the 
inheritance  of  a  fluctuation  variate  and  of  Mendelian  segregation  (Lutz, 
1908) .  In  my  report  at  the  time  of  finishing  the  work  at  Cold  Spring 
Harbor  I  even  constructed  hypothetical  curves  for  this  variation.  How- 
ever, I  have  since  realized  that  the  "explanation  "  of  conditions  6  and 
7  was  very  weak.  It  was  ' '  that  in  selecting  parents  to  continue  the 
normal  strain  I  merely  selected  flies  having  no  extra  veins.  For  the 
most  of  the  time  the  work  of  describing  offspring  was  unavoidably  so 
far  behind  the  breeding-work  that  I  did  not  know  what  percentage  of 
their  brothers  and  sisters  were  abnormal.  Hence  I  had  no  way  of  judg- 
ing as  to  the  germinal  constitution  of  the  parents.  The  normal  strain 
is  probably  a  mixture  of  flies  lacking  the  abnormal  factor  (might  be 
called  NN's)  and  of  flies  which  have  it  in  hybrid  condition  of  weak 
allelomorphic  strength  (NA's).  In  generations  vn  to  xxn  I  was  prob- 
ably unconsciously  breeding  from  these  NA's.  This  is  an  answer  to 
the  first  part  of  condition  6. 


22 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


generation. 


Mating 
No. 

Ab- 
normal. 

Total. 

Per  cent 
abnormal. 

2561   .  ... 
2562 

43 

42 
65 
47 
21 
19 
14 

113 

126 
130 
79 
28 
27 
24 

38.1 
33.3 
50.0 
59.5 
75.0 
70.4 
58.3 

2629 

2630 

2631 

2633 

2645 

Total... 

251 

527 

47.6 

"We  have,  now,  only  to  take  up  the  fact  that  in  inheritance  these 
abnormalities  follow  the  spirit  but  not  the  letter  of  the  Mendelian  law 
(condition  7) .  We  might  consider  that  the  dominance  of  normal  over 
abnormal  is  merely  due  to  the  dilution  of  the  abnormality-producing 
factor  in  the  NA's.  If  it  is  strong  it  may  be  potent  enough  to  produce 
abnormalities  in  spite  of  this  dilu- 

firm   fVmco-ivino-inrwnnlpfpdoTni-     Table  23-— Results  of  seven  crosses  between 
tion,  tnus  giving  incomplete  aomi  abnormal  and  normal  strains  in  a  late 

nance.  Even  when  it  is  pure 
(AA),  its  fluctuation  may  give 
individuals  in  which  the  zygotic 
strength  is  not  great  enough  to 
produce  abnormalities,  thus  ac- 
counting for  the  normals  in  the 
abnormal  strain.  Whether  one 
could  so  increase  the  strength  of 
the  abnormality-producing  factor 
that  when  the  selected  flies  are 
mated  with  flies  lacking  the  factor 
all  the  offspring  will  be  abnormal  is  not  certain,  but  table  23  indicates 
such  a  possibility. ' ' 

If,  however,  we  have,  in  carefully  conducted  experiments,  many  flies 
somatically  normal  but  germinally  abnormal,  and  if  by  selection  it  is 
easy  to  so  weaken  the  abnormality-producing  factor  that  from  a  strain 
100  per  cent  abnormal  we  get  and  keep  one  100  per  cent  somatically 
normal  (all  presumably  germinally  abnormal,  since  they  came  from  a 
100  per  cent  abnormal  strain) ,  must  we  not  admit  the  possibility  that  all 
somatically  normal  flies  have  the  germinal  possibilities  of  abnormality? 
This  makes  the  problem  much  simpler,  as,  leaving  out  the  question  of 
Mendelian  segregation,  we  have  only  to  consider  the  inheritance  of  the 
variations  of  an  abnormality-producing  factor,  whatever  that  may  be. 
Let  us  take  up  the  seven  conditions  which  must  be  satisfied. 

Condition  1. — All  flies  possess  the  abnormality-producing  factor  in  the 
germ.  It  is  usually  so  weak  that  it  has  no  visible  effect  upon  the  soma. 
Occasionally,  however,  it  is  strong  enough  to  do  so,  and  its  strength 
can  be  so  increased  by  selection  that  it  always  does  so. 

Condition  2.  —It  is  necessary  to  suppose  that  it  takes  a  greater  strength 
of  the  germinal  factor  to  have  a  visible  effect  upon  the  male  soma  than 
upon  the  female.  This  sexual  difference  of  developmental  physiology 
is  quite  common  and  the  hypothesis  will  doubtless  be  readily  allowed 
by  most  critics  in  this  case.  It  is  interesting  to  wonder  whether  the 
possession  of  horns  by  certain  male  ungulates,  while  the  females  lack 
them,  is  an  extreme  example  of  this  same  phenomenon. 

Condition  3.  —To  be  expected  on  this  hypothesis. 

Condition  U—  The  explanation  here  would  differ  according  to  different 
notions  of  the  mechanics  of  heredity.    If  we  accept  the  apparently  most 


INHERITANCE  OF  ABNORMAL  VENATION.  23 

favored  notion  that  there  is  some  specific  substance  in  the  germ  which 
produces  the  character  in  question  and  which  is  divided  at  the  cell- 
division  which  separates  the  substances  forming  the  right  side  from 
those  forming  the  left  side  of  the  complete  soma,  it  would  be  difficult  to 
believe  the  division  is  always,  or  in  most  cases,  exactly  even.  If  it  is  not 
with  respect  to  the  abnormality-producing  factor,  it  would  give  rise  to 
the  phenomenon  of  asymmetry  as  to  the  extent  of  the  abnormality. 
Only  when  the  factor  is  rather  weak  to  start  with  would  this  deviation 
from  exact  equality  of  division  frequently  result  in  the  share  going  to 
one  wing  being  so  small  that  that  wing  would  be  normal  while  the  other 
wing  is  abnormal;  hence  there  would  be  a  correlation  between  the 
degree  of  the  abnormality  and  the  phenomenon  of  one  wing  being  normal 
while  the  other  is  abnormal  (see  p.  5) .  The  approximate  equality  of 
the  apportionment  of  the  factor  in  division  may  be  taken  as  the  expla- 
nation of  the  correlation  in  the  intensity  of  the  abnormality  in  the  two 
wings,  and  the  degree  of  this  correlation  is  a  measure  of  the  degree  of 
equality  of  the  division.  Since  the  going  of  a  slightly  greater  strength 
to  the  right  side  than  to  the  left,  or  vice  versa,  is  a  mere  accident  in 
development,  it  is  not  to  be  expected  that  there  will  be  an  inheritance 
of  a  particular  side  getting  the  greater  strength  (see  p.  17).  But  since 
flies  abnormal  in  only  one  wing  came  from  germs  which  had  a  weak 
abnormality-producing  factor,  it  is  to  be  expected  that  the  germs  they 
produce  will  be  weak  with  respect  to  this  factor,  and  so  a  smaller  per- 
centage of  their  offspring  will  be  abnormal  than  of  the  offspring  of 
parents  abnormal  in  both  wings  (see  p.  17). 

Condition  5.— Since  it  takes  a  greater  strength  of  the  germinal  factor 
to  produce  abnormalities  in  the  males  than  in  the  females,  a  male 
somatically  normal  may  be  produced  by  and  produce  germs  containing 
as  strong  or  stronger  abnormality  factors  than  a  female  which  is  somat- 
ically abnormal.  Hence,  in  the  long  run,  normal  male  X  abnormal 
female  will  give  more  abnormal  offspring  than  abnormal  male  X  normal 
female,  because  in  the  latter  cross  one  of  the  parents  (the  female)  neces- 
sarily has  the  factor  very  weak. 

Condition  6.— "In  selecting  parents  to  continue  the  normal  strain,  I 
merely  selected  flies  having  no  extra  veins.  For  the  most  of  the  time 
the  work  of  describing  offspring  was  unavoidably  so  far  behind  the 
mating  work  that  I  did  not  know  what  percentage  of  their  brothers  and 
sisters  were  abnormal.  Hence  I  had  no  way  of  judging  as  to  the  ger- 
minal constitution  of  the  parents."  Being  unable,  by  examination  of 
the  soma,  to  tell  the  exact  strength  of  the  germinal  content,  I  uncon- 
sciously used  as  parents  flies  in  which  the  abnormality-producing  factor 
was  relatively  strong,  and  thus  started  and  for  a  time  maintained  a 
strain  giving  a  relatively  large  number  of  abnormal  flies.  When  the 
flies  were  allowed  to  do  their  own  selecting  of  mates  they  were  more 
successful  (see  p.  36) . 


24  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

Condition  7.—  From  all  we  know  of  the  inheritance  of  fluctuating 
variations,  the  mating  of  one  grade  with  another  will  give  variations 
about  a  mid-grade.  If  it  takes  a  certain  grade  or  strength  of  the  germ- 
inal factor  to  produce  a  somatic  effect  and  we  mate  a  low  grade  (somati- 
cally normal)  with  one  just  sufficient  to  produce  somatic  abnormalities, 
the  variations  about  the  mid-grade  will,  in  most  cases,  be  too  low  to 
produce  visible  abnormalities.  In  other  words,  normality  will  dominate 
over  abnormality.  If,  however,  the  parents  are  such  that  the  grades 
of  the  offspring  are  about  that  required  to  produce  somatic  effects,  the 
dominance  will  be  imperfect.  The  abnormality  will  appear  to  be  obey- 
ing "the  spirit  of  the  Mendelian  law,"  but  it  will  naturally  "pay  little 
attention  to  the  letter  of  the  simple  law  or  any  of  the  modifying  clauses, " 
especially  in  the  latter  generations,  where  the  abnormal  strain  had  the 
germinal  factor  much  strengthened  by  selection. 

It  seems  to  me,  then,  that  if  we  accept  the  notion  of  some  specific 
factor  in  the  germ  which  brings  about  the  details  of  the  characters  of  the 
soma  the  facts  here  discussed  may  be  considered  to  be  the  result  of  the 
action  of  a  factor  present  in  all  germs.  The  strength  of  this  factor 
varies,  and  when  of  a  certain  strength  produces  certain  visible  effects. 
The  partial  dominance  of  normal  over  abnormal  is  due  to  the  mean  con- 
dition of  the  factor  in  the  offspring  of 

(flies  with  factor  strong  enough  to  produce  extra  veins)  x  (flies  with  factor  weak) 

usually  being  below  the  strength  required  to  produce  abnormality. 

I  have  not  taken  up  the  resemblance  of  the  behavior  of  these  abnor- 
malities to  that  of  ' '  ever-sporting  varieties, ' '  because  I  feel  that  classing 
these  as  such  would  not  be  a  step  toward  an  explanation.  It  would 
merely  be  naming  the  difficulty.  It  is  also  not  the  intention  to  imply 
that  this  hypothesis  would  apply  to  those  other  cases  which  are  trouble- 
some from  a  Mendelian  standpoint  and  to  which  the  principle  of  vary- 
ing potency  of  Mendelian  determiners  has  been  applied  (for  example, 
Davenport,  1910).  It  seems  not  only  possible  but  probable  that  many 
apparently  non-Mendelian  cases  may  be  explained  as  a  combination  of 
alternative  and  blending  inheritance  (Lutz,  1908).  But  a  simpler  and 
more  probable  explanation  of  these  data,  provided  we  accept  the  some- 
what dubious  "germinal  factor  "  idea,  seems  to  be  that  we  are  dealing 
here  solely  with  a  fluctuating  character— the  strength  of  the  abnormality- 
producing  factor— and  that  the  study  of  its  inheritance  is  made  difficult, 
if  not  largely  impossible,  by  the  fact  that  only  in  the  upper  part  of  its 
range  can  we  judge  of  the  relative  values  of  this  variable,  for  in  the 
lower  part  its  effects  are  invisible. 


INHERITANCE  OF  ABNORMAL  VENATION. 


25 


Table  24.—  Percentage  of  abnormal  offspring  in  48  matin qa 
ofNl  (ex.  Ni  X  N2)  X  N9  (ex.  Ni  X  M>). 


F KM  ALES. 


0 

5 

15 

25 

30 

45 

55 

05 

75 

95 

0 

26 

8 

1 

5 

4 

1 

15 

1 

1 

1 

25 

1 

2 

1 

1 

35 

45 

55 

65 

75 

85 

95 

Table  25. — Percentage  of  abnormal  offspring  in  5  matings  of 
Nt  (ex.  A6  X  A?)  X  N?  {ex.  Ai  X  4s). 


FEMALES. 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

3 

5 

1 

1 

15 

25 

35 

45 

55 

65 

75 

85 

95 

26 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


Table  26.—  Percentage  of  abnormal  offspring  in  6  matings  of 
NS   (ex.  At  X  Ni)  X  M  {ex.  A$  X  N9). 


FEMALES. 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

5 

1 

15 

1 

2 

25 

1 

1 

35 

45 

55 

65 

75 

85 

95 

Table  27.—  Percentage  of  abnormal  offspring  in  U  matings  of 
Ns  (ex.  Ns  X  Ai)  X  iV?  (ex.Ns  X  A$). 


FEMALES 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

I 

5 

15 

25 

35 

1 

1 

45 

1 

55 

65 
75 

85 

95 

INHERITANCE  OF  ABNORMAL  VENATION. 


27 


Table  28. — Percentage  of  abnormal  offspring  in  5  matings  oj 
Ns  (ex.  Ns  X  N2)  X  A?  (ex.  Ns  X  As). 


FEMALES. 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

1 

5 

1 

1 

15 

25 

35 

1 

45 

1 

55 

65 

75 

85 

95 

Table  29.—  Percentage  of  abnormal  offspring  in  7  mating*  of 
Ns  (ex.  Ns  X  N9)  X  A2  (ex.  As  X  At). 


FEMALES- 


0 

5 

15 

25 

35 

45 

55 

65 

75  85  1  95 

> 

0 

1 

5 
15 
25 

1 

1 

1 

1 

35 

1 

1 

45 

55 

65 

75 

85 

, 

95 

28 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


Table  30. — Percentage  of  abnormal  offspring  in  IS  matings 
of  Ns  (ex.  NsXAl)   X  A?  (ex.  NSXA2). 


FEMALES. 


0 

5 

15 

25 

35  45 

55 

65 

75  85  95 

0 

1   1 

5 

15 

25 

1 

35 

1 

1 

1 

45 

1 

2 

1 

55 

65 

2 

75 

1 

85 

1 

95 

1 

Table  31.—  Percentage  of  abnormal  offspring  in  9  matings  of 
Ns  (ex.  As  X  As)  X  4$  (ex.  As  X  At). 


FEMALES 


0 

5 

15 

25 

35 

45 

55  |  65 

75  85 

95 

0 

5 

15 

25 

35 

45 

1 

55 

1 

65 

75 

1 

1 

85 

1 

95 

4 

INHERITANCE  OF  ABNORMAL  VENATION. 


29 


TABLE  32. — Percentage  of  abnormal  offspring  in  6  matings  of 
As  (ex.  As  X  A9)  XN2  (ex.  Ns  X  M>). 


FEMALES- 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

5 

1 

3 

1 

15 

25 

35 

45 

55 

65 

1 

75 

85 

95 

Table  33. — Percentage  of  abnormal  offspring  in  12  matings 
of  As  (ex.  As  X  N9)  X  M>  (ex.  As  X  Ni). 


FEMALES. 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

1 

5 

1 

1 

15 

1 

25 

1 

35 

1 

45 

55 

1 

65 

1 

75 

2 

1 

1 

85 

95 

. 

30 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


Table  34. — Percentage  of  abnormal  offspring  in  21  matings 
of  AS  (ex.  Ns  X  Ai)   X  Al  {ex.  Ns  X  A9). 


FEMALES. 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

1 

5 

15 

25 

35 

2 

1 

1 

45 

2 

1 

55 

1 

2 

1 

65 

1 

2 

75 

1 

2 

85 

95 

3 

Table  35. — Percentage  of  abnormal  offspring  in  45  matings 
of  A6  (ex.  As  X  A$)  X  A2  (ex.  As  X  A$). 


lXMALES. 


0 

5 

15 

25 

35 

45 

55 

65 

75 

85 

95 

0 

5 

15 

25 

35 

45 

55 

1 

65 

1 

75 

1 

85 

1 

5 

95 

36 

INHERITANCE  OF  ABNORMAL  VENATION. 


31 


Table  36. — Percentage  of  abnormal  offspring  of  200  families. 


Oflapring. 

Parents 

Mating 
No. 

Male. 

Female. 

Total 

Father. 

Mother. 

No. 
recorded. 

P.  ct. 

abnormal. 

No. 
recorded. 

P.ct 
ibnormaL 

]'.  ct 
abnormal. 

211 

A  205 

A  205 

75 

30.7 

102 

64.7 

50.3 

214 

N205 

N205 

39 

30.8 

34 

47.1 

38.4 

220 

A  207 

N207 

11 

0.0 

8 

0.0 

0.0 

226 

A  205 

A  205 

69 

46.4 

77 

80.5 

64.4 

230 

A  205 

A  210 

38 

84.2 

27 

85.2 

84.6 

233 

A  210 

A  210 

31 

71.0 

25 

76.0 

73.2 

238 

A  210 

A  210 

22 

36.4 

23 

52.2 

44.4 

239 

N211 

N210 

29 

51.7 

29 

69.0 

60.3 

241 

N216 

N216 

61 

0.0 

69 

0.0 

0.0 

242 

N216 

N216 

55 

0.0 

63 

3.2 

1.7 

243 

N214 

N214 

64 

28.1 

57 

36.8 

32.2 

245 

N215 

N215 

20 

20.0 

14 

42.9 

29.4 

246 

N215 

N215 

27 

25.9 

31 

32.3 

29.3 

247 

N215 

N215 

37 

29.7 

27 

40.7 

34. 4 

253 

N220 

N220 

13 

0.0 

16 

0.0 

0.0 

257 

N211 

A  211 

87 

70.1 

90 

70.0 

70.0 

258 

N211 

A  211 

47 

93.6 

63 

96.8 

95.5 

259 

N211 

A  211 

21 

47.6 

35 

94.3 

76.8 

273 

N242 

N242 

10 

0.0 

16 

0.0 

0.0 

276 

A  246 

N246 

18 

11.1 

23 

34.8 

24.4 

278 

N246 

N246 

16 

25.0 

17 

58.8 

42.4 

280 

N253 

N253 

10 

0.0 

20 

0.0 

0.0 

281 

N253 

N253 

37 

2.7 

52 

1.9 

22 

283 

A  257 

A  257 

47 

38.3 

54 

83.3 

62.4 

284 

A  257 

A  257 

77 

62.3 

91 

95.6 

80.4 

285 

N257 

A  257 

72 

43.1 

72 

94.4 

68.8 

286 

A  257 

A  257 

34 

44.1 

36 

88.9 

67.1 

288 

A  258 

A  258 

62 

54.8 

67 

95.5 

76.0 

289 

A  258 

N258 

43 

46.5 

38 

97.4 

70.4 

291 

A  258 

A  258 

44 

65.9 

66 

93.9 

82.7 

292 

A  258 

A  258 

16 

37.5 

27 

92.6 

72.1 

294 

N241 

N241 

16 

0.0 

19 

0.0 

0.0 

297 

N246 

N241 

34 

2.9 

57 

10.5 

7.7 

298 

N246 

A  259 

43 

48.8 

55 

76.4 

64.3 

299 

A  238 

A  259 

26 

73.1 

28 

96.4 

85.2 

301 

N257 

N258 

53 

32.1 

51 

76.5 

53.8 

302 

N257 

A  258 

56 

51.8 

41 

92.7 

69.1 

305 

N241 

A  233 

26 

0.0 

29 

3.4 

1.8 

316 

N276 

N225 

25 

0.0 

40 

0.0 

(Ml 

317 

N225 

A  289 

25 

16.0 

25 

4.0 

10.0 

318 

A  288 

N225 

32 

6.3 

48 

0.0 

2.5 

319 

A  283 

N225 

30 

3.3 

42 

7.1 

5.6 

320 

A  284 

N225 

50 

10.0 

60 

20.0 

15.6 

321 

A  284 

N225 

27 

7.4 

39 

2.6 

4.5 

322 

A  284 

N225 

48 

6.3 

53 

9.4 

7.9 

323 

N297 

N297 

29 

10.3 

35 

14.3 

12. 5 

328 

N284 

A  284 

28 

92.9 

26 

96.2 

94.4 

330 

N284 

A  284 

48 

95.8 

66 

90.9 

930 

331 

N284 

A  284 

33 

78.8 

28 

S2.1 

80.3 

333 

A  285 

A  285 

27 

59.3 

26 

84.6 

71.7 

338 

A  285 

A  285 

26 

53.8 

29 

62.1 

58. 2 

339 

N285 

A  285 

34 

91.2 

45 

75.6 

82. 3 

.     i      1 

341 

N288 

A  288 

20 

90.0 

25 

92.0 

91  1 

342 

N294 

A  284 

38 

31.6 

52 

346 

33.3 
36.6 
295 

12.4 
253 

343 
344 
345 
347 

N297 
N273 
N273 
N320 

A  284 
A  284 
A  288 
N320 

35 
42 
58 
32 

25.7 
14.3 
37.9 
28.1 

47 
63 
41 
55 

44.7 
39.7 
48.8 
236 

1 

32 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


Table  36. — Percentage  of  at 

mormal  oj. 

7 spring  of 

200  famil 

ies — Cont 

inued. 

T^O  fVknttl 

Oflspring. 

Mating 
No. 

JrHr* 

Male. 

Female. 

Total 
p.  ct. 

abnormal. 

Father. 

Mother. 

No. 
recorded. 

P.  ct. 
abnormal. 

No. 
recorded. 

P.  ct. 
abnormal. 

348 

N320 

N320 

31 

19.4 

37 

21.6 

20.6 

349 

A  320 

N320 

57 

36.8 

65 

38.5 

37.7 

350 

N320 

N320 

37 

13.5 

49 

28.6 

22.1 

351 

N320 

A  320 

36 

19.4 

32 

31.3 

25.0 

353 

N320 

N320 

37 

10.8 

24 

16.7 

13.1 

354 

A  284 

N320 

37 

45.9 

41 

63.4 

55.1 

355 

A  284 

N321 

44 

2.3 

51 

21.6 

12.6 

356 

A  284 

N322 

38 

28.9 

30 

60.0 

42.6 

357 

N318 

N318 

32 

3.1 

35 

11.4 

7.5 

358 

A  318 

N322 

28 

0.0 

48 

2.1 

1.3 

359 

A  318 

N322 

43 

2.3 

33 

9.1 

5.3 

364 

N317 

N317 

24 

0.0 

24 

0.0 

0.0 

365 

N345 

A  345 

44 

36.4 

52 

67.3 

53.1 

366 

N342 

A  342 

39 

30.8 

50 

42.0 

37.1 

367 

N330 

A  330 

42 

64.3 

80 

91.3 

81.9 

368 

N330 

A  330 

43 

48.8 

55 

87.3 

70.4 

369 

N339 

A  339 

32 

34.4 

42 

76.2 

58.1 

372 

N338 

A  338 

36 

58.3 

37 

89.2 

74.0 

375 

N344 

A  344 

29 

24.1 

36 

52.8 

40.0 

377 

N344 

A  330 

23 

60.9 

30 

93.3 

79.2 

379 

A  349 

N349 

68 

70.6 

58 

70.7 

70.6 

380 

A  349 

N349 

26 

15.4 

29 

24.1 

20.0 

383 

A  349 

N349 

35 

25.7 

37 

59.5 

43.1 

384 

A  349 

N349 

27 

63.0 

34 

88.2 

77.0 

387 

N368 

A  368 

32 

84.4 

36 

83.3 

83.8 

388 

A  349 

N349 

23 

4.3 

25 

12.0 

8.3 

399 

N367 

A  367 

20 

50.0 

23 

95.7 

74.4 

401 

A  367 

A  367 

52 

92.3 

61 

93.4 

92.9 

402 

A  367 

A  367 

103 

76.7 

90 

94.4 

85.0 

404 

A  367 

A  367 

66 

60.6 

67 

64.2 

62.4 

405 

A  367 

A  367 

9 

0.0 

16 

0.0 

0.0 

406 

A  367 

A  367 

56 

58.9 

76 

86.8 

75.0 

408 

A  367 

A  367 

13 

100.0 

16 

100.0 

100.0 

409 

A  367 

A  367 

51 

43.1 

49 

93.9 

68.0 

411 

A  367 

A  367 

23 

78.3 

39 

82.1 

80.6 

414 

N405 

N405 

56 

0.0 

69 

0.0 

0-0 

415 

N405 

N405 

75 

0.0 

74 

0.0 

0.0 

417 

N405 

N405 

38 

0.0 

73 

0.0 

0.0 

418 

A  379 

N379 

32 

71.9 

33 

75.8 

73  8 

419 

A  379 

N379 

35 

77.1 

22 

100.0 

83.0 

433 

N399 

A  399 

24 

70.8 

17 

88.2 

78.0 

436 

A  379 

N379 

20 

75.0 

36 

88.9 

83.9 

439 

A  408 

A  408 

54 

85.2 

53 

81.1 

83.2 

440 

A  408 

A  408 

25 

96.0 

26 

100.0 

98.0 

453 

Nwild 

A  399 

65 

1.5 

83 

2.4 

2.0 

454 

Nwild 

A  399 

49 

0.0 

52 

0.0 

0.0 

455 

Nwild 

A  399 

41 

36.6 

32 

34.4 

35.6 

456 

Nwild 

A  399 

42 

4.8 

59 

10.2 

7.9 

459 

A  wild 

Nwild 

49 

2.0 

59 

15.3 

9.3 

474 

N414 

N414 

18 

0.0 

15 

0.0 

0.0 

513 

A  439 

A  439 

13 

92.3 

10 

100.0 

95.7 

514 

A  440 

A  440 

44 

97.7 

44 

97.7 

97.7 

523 

N474 

N474 

39 

0.0 

37 

0.0 

0.0 

533 

A  513 

A  513 

44 

95.5 

54 

100.0 

98.0 

548 

A  514 

A  514 

26 

96.2 

37 

100.0 

98.4 

557 

A  548 

A  548 

18 

94.4 

29 

100.0 

97.9 

564 

A  533 

A  533 

4 

100.0 

4 

100.0 

100.0 

575 

N523 

N523 

39 

0.0 

20 

0.0 

0.0 

INHERITANCE   OF  ABNORMAL  VENATION. 


33 


Table  36. — Percentage  of  abnormal  offspring  of  200  families — Continued. 


Iflfepring. 

Pn  rppt^ 

Mating 

No. 

lalrl 

Male. 

Female. 

Total 

p.  ii. 
abnormal, 

Father. 

Mother. 

No. 
recorded. 

P.  ct 
ibnormaL 

No. 

recorded. 

i 

P.et. 
ibnormaL 

576 

N523 

N523 

52 

0.0 

48 

0.0 

ii  ii 

582 

N575 

N575 

28 

0.0 

87 

0.0 

0.0 

584 

N557 

A  557 

18 

100.0 

24 

100.0 

100.0 

585 

N576 

A  557 

48 

4.2 

45 

24.4 

14.0 

587 

N576 

N576 

29 

0.0 

21 

4.8 

20 

588 

N576 

N576 

55 

0.0 

46 

0.0 

589 

A  564 

A  564 

24 

100.0 

20 

100.0 

100.0 

590 

N588 

N582 

48 

0.0 

55 

0.0 

0.0 

591 

N588 

N588 

1 

0.0 

3 

0.0 

0.0 

592 

N587 

N582 

32 

0.0 

33 

0.0 

0.0 

593 

N587 

N582 

39 

0.0 

36 

0.0 

0.0 

594 

N585 

N585 

73 

41.1 

69 

62.3 

51.4 

600 

N588 

N588 

55 

0.0 

58 

0.0 

602 

A  589 

A  589 

21 

100.0 

25 

100.0 

1000 

605 

A  584 

A  585 

30 

40.0 

37 

67.6 

55.2 

606 

A  584 

A  584 

2 

100.0 

7 

100.0 

100 

611 

A  585 

A"C" 

45 

17.8 

50 

38.0 

28.4 

613 

N592 

N592 

38 

0.0 

53 

1.9 

1.1 

614 

N593 

N590 

38 

0.0 

50 

2.1 

1.1 

622 

N600 

N591 

19 

0.0 

45 

4.4 

3.1 

623 

N600 

N591 

24 

0.0 

35 

0.0 

0.0 

626 

A  602 

A  594 

53 

32.1 

60 

53.3 

43.1 

632 

A  606 

A  606 

22 

100.0 

19 

100.0 

100.0 

633 

A  602 

A  611 

11 

90.9 

14 

92.9 

92.0 

639 

A  594 

A  602 

1 

100.0 

7 

100.0 

100.0 

641 

A  611 

A  605 

32 

87.5 

49 

95.9 

92.6 

642 

A  605 

A  605 

34 

55.9 

43 

651 

61.0 

643 

A  611 

A  611 

3 

100.0 

4 

100.0 

100.0 

657 

N614 

N614 

31 

0.0 

30 

0.0 

0.0 

660 

N622 

N622 

44 

2.3 

40 

5.0 

8.6 

663 

N623 

N623 

42 

0.0 

29 

0.0 

0.0 

665 

N613 

N622 

19 

0.0 

64 

0.0 

0.0 

670 

A  626 

A  602 

35 

88.6 

45 

100.0 

95.0 

677 

A  641 

A  626 

23 

95.7 

23 

100.0 

97.8 

678 

A  633 

A  633 

9 

100.0 

5 

100.0 

100.0 

680 

A  642 

A  642 

34 

97.1 

49 

100.0 

98.8 

681 

A  639 

A  639 

10 

70.0 

21 

100.0 

90.3 

682 

A  626 

A  626 

34 

91.2 

41 

100.0 

96.0 

685 

A  643 

A  633 

18 

83.3 

23 

100.0 

92.7 

692 

A  633 

A  633 

29 

93.1 

30 

96.7 

W.9 

694 

A  642 

A  632 

29 

75.9 

31 

83.9 

80.0 

710 

N660 

N657 

27 

0.0 

35 

0.0 

0.0 

715 

N665 

N663 

13 

0.0 

24 

0.0 

0.0 

719 

A  670 

A  677 

7 

100.0 

11 

100.0 

100.0 

723 

A  685 

A  682 

24 

95.8 

27 

100.0 

98. 0 

726 

A  678 

A  680 

43 

90.7 

54 

100.0 

95. 9 

727 

A  692 

A  692 

11 

100.0 

15 

100.0 

loi). 0 

729 

A  681 

A  682 

.  •  ■ 

1 

100. 0 

100.0 

737 

A  694 

A  694 

9 

88.9 

7 

100.0 

93. 8 

752 

A  726 

A  719 

45 

100.0 

56 

100.0 

1000 

753 

A  726 

A  723 

27 

92.6 

27 

100.0 

96. 3 

763 

A  727 

A  727 

12 

100.0 

13 

11  III  II 

100. 0 

764 

A  726 

A  727 

29 

96.6 

29 

100.0 

98 

765 

A  726 

A  729 

46 

97.8 

50 

100.0 

99  0 

767 

A  737 

A  737 

20 

80.0 

27 

10U  0 

;»l  .6 

785 
799 

N715 
A  753 

N715 
A  753 

63 
17 

20.6 
88.2 

83 
38 

20.5 

20.5 

90.9 

0.0 

802 

N715 

N710 

40 

0.0 

44 

0.0 

34 


EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 


Table  36. — Percentage  oj  abnormal  offspring  of  200  families— Continued. 


Offspring 

Par**1 

Mating 
No. 

Male. 

Female. 

Total 

Father. 

Mother. 

No. 
recorded. 

P.  ct. 
abnormal 

No. 
.    recorded. 

P.  ct. 
abnormal 

p.  ct. 
abnormal. 

804 

N710 

N715 

19 

0.0 

19 

5.3 

2.6 

808 

A  752 

A  765 

21 

95.2 

25 

100.0 

97.8 

813 

A  763 

A  763 

8 

100.0 

9 

100.0 

100.0 

816 

A  764 

A  764 

26 

100.0 

23 

100.0 

100.0 

818 

A  767 

A  767 

13 

100.0 

12 

100.0 

100.0 

831 

N804 

N802 

34 

0.0 

35 

0.0 

0.0 

833 

N802 

N802 

40 

0.0 

53 

1.9 

1.1 

836 

N785 

N785 

46 

19.6 

63 

38.1 

30.3 

851 

A  799 

A  799 

6 

100.0 

11 

100.0 

100.0 

853 

A  816 

A  808 

25 

100.0 

41 

100.0 

100.0 

858 

A  808 

A  808 

38 

100.0 

36 

100.0 

100.0 

880 

N836 

N831 

52 

5.8 

83 

7.2 

6.7 

882 

N833 

N836 

55 

o.o 

55 

3.6 

1.8 

886 

A  851 

A  853 

29 

100.0 

44 

100.0 

100.0 

889 

A  858 

A  853 

16 

87.5 

35 

97.1 

94.1 

898 

N857 

N857 

55 

3.6 

63 

1.6 

2.5 

899 

N857 

N857 

50 

2.0 

33 

0.0 

1.2 

900 

A  857 

N857 

38 

2.6 

44 

13.6 

8.5 

902 

A  886 

A  889 

28 

100.0 

36 

97.2 

98.4 

907 

A  886 

A  886 

37 

100.0 

27 

100.0 

100.0 

908 

A  886 

A  886 

42 

100.0 

55 

100.0 

100.0 

917 

A  886 

A  886 

39 

100- 0 

39 

100.0 

100.0 

926 

N880 

N880 

49 

6.1 

50 

6.0 

6-1 

XXII 

A  886 

N882 

20 

65.0 

27 

74.1 

70- 2 

943 

A  902 

A  902 

59 

98.3 

74 

100.0 

99.2 

946 

A  xxn 

A  xxn 

44 

40.9 

62 

62.9 

53.8 

947 

A  xxn 

N  xxn 

50 

52.0 

78 

66.7 

60.9 

948 

N  xxn 

N  xxn 

54 

25.9 

59 

40.7 

36. 9 

953 

N926 

N926 

40 

0.0 

58 

13.8 

8-2 

954 

N926 

A  908 

43 

32.6 

46 

58.7 

46.1 

955 

N926 

A  908 

40 

27.5 

53 

26.4 

26.9 

967 

A  XXII 

A  xxn 

37 

54.1 

46 

71.7 

63.9 

968 

A  xxn 

A  xxn 

23 

87.0 

32 

100.0 

94.5 

970 

N  xxn 

N  xxn 

44 

31.8 

43 

34.9 

33.3 

983 

N946 

N946 

46 

39.1 

43 

60.5 

49.4 

984 

A  946 

A  946 

33 

81.8 

51 

90.2 

86.9 

985 

A  946 

N946 

41 

56.1 

41 

78.0 

67.1 

986 

N947 

N947 

29 

24.1 

36 

389 

32.3 

989 

A  947 

N947 

27 

66.7 

29 

82.8 

75.0 

997 

A  943     | 

A  943 

27 

77.8 

28 

85.7 

81.8 

1006 

A  930 

N957 

18 

55.5 

20 

60.0 

57.9 

1017 

N953 

N953 

7 

0.0 

8 

12.5 

7  3 

1021 

A  947 

N947 

21 

47.6 

22 

45.5 

1  ■  o 

46.5 

1064 
1069 

N997 
N1017 

A  997 
N1017 

30 
24 

50.0 
0.0 

38 
40 

78.9 
2.5 

66.2 
1  6 

1071 

A  981 

N1006 

4 

0.0 

7 

14  3 

9.1 

0.0 

35.1 

32.2 

0.0 

0.0 

9.3 

1.4 

4.1 

5.4 

12.5 

17.0 

15.2 

2.2 

10.7 

1111 

N1062 

N1069 

9 

0.0 

9 

0  0 

1117 

N1064 

N1064 

19 

26.3 

18 

44 

1118 
1123 

N1064 
N1069 

N1064 
N1069 

55 
52 

23.4 
0.0 

63 
65 

39.7 
0.0 
0  0 

1124 

N1069 

N1069 

19 

0.0 

36 

1141 
1153 

2  A 1102 
Nllll 

3  N 1071 
Nllll 

39 
69 

10.3 
0.0 

58 
74 

8.6 

2.7 

6.4 

5.7 

16.7 

20.7 

21.4 

1.4 

13.6 

1154 
1156 
1158 
1166 
1172 
1176 
1177 

Nllll 
Nllll 
N1117 
N1158 
N1156 
N1154 
N1154 

Nllll 
Nllll 
N1118 
N1158 
N1156 
N1156 
N1156 

51 
39 
2 
42 
37 
70 
53 

2.0 
5  1 
0.0 
11.9 
8.1 
2.9 
7.5 

47 

53 

6 

58 
42 
69 
59 

INHERITANCE  OF  ABNORMAL  VENATION. 


36 


TABLE  36. — Percentage  of  abnormal  offspring  of  200  families — Continued. 


P'l  »»£in4o 

Offspring. 

Mating 
No. 

l  rtl  tr 

Male. 

female. 

L.tal 

Father. 

Mother. 

recorded. 

P.ct 
abnormal. 

recorded. 

1-.  d 
abnormal. 

p.  ct 
ibnorm&L 

1181 

A 1141 

4  N 1141 

39 

10.3 

70 

J2.9 

18.3 

1190 

2  A 1141 

4  N 1141 

45 

11.1 

53 

11.3 

11.2 

1192 

N1177 

N1177 

39 

2.6 

28 

17.9 

!»  0 

1193 

N1177 

N1177 

49 

2.0 

73 

13 

1.6 

1197 

N1176 

N1176 

61 

0.0 

53 

1.9 

0.9 

1204 

N1166 

N1166 

2 

0.0 

6 

o.o 

0.0 

1208 

A 1181 

3  N 1181 

49 

8.2 

53 

11.3 

9.8 

1213 

N1166 

N1166 

33 

3.0 

17 

23.4 

15. 0 

1217 

3  A 1190 

4  N 1190 

28 

21.4 

29 

114 

31.6 

1221 

N1197 

N1197 

43 

4.7 

47 

64 

5.6 

1226 

N1193 

N1193 

29 

0.0 

21 

9.5 

4.0 

1229 

N1204 

N1204 

5 

0.0 

11 

00 

0.0 

1254 

N1229 

N1229 

23 

0.0 

21 

0.0 

0.0 

1256 

N1226 

N1226 

39 

2.6 

46 

10.9 

7.1 

1266 

N1254 

N 1254 

25 

4.0 

26 

3.8 

39 

1268 

N 1254 

N1254 

13 

0.0 

12 

0.0 

0.0 

1269 

N1254 

N1254 

4 

0.0 

9 

0.0 

0.0 

1282 

N1256 

N1256 

4 

0.0 

4 

0.0 

0.0 

1286 

N1269 

N1269 

27 

0.0 

29 

0.0 

0.0 

1293 

N1286 

N1286 

55 

1.8 

53 

5.7 

3.7 

1300 

N1282 

N 1282 

20 

0.0 

24 

0.0 

0.0 

1309 

N1293 

N  1293 

12 

0.0 

14 

0.0 

1327 

N1300 

N1300 

52 

0.0 

48 

0.0 

00 

1347 

N1327 

N1327 

46 

0.0 

59 

0.0 

0.0 

1394 

N1347 

N1347 

61 

0.0 

73 

0.0 

0.0 

1428 

3  N 1394 

3  N 1394 

62 

1.6 

66 

0.0 

0.8 

1454 

N1428 

N1428 

65 

0.0 

64 

0.0 

0.0 

1476 

N1454 

N1454 

43 

0.0 

46 

0.0 

0.0 

1533 

N1476 

N1476 

34 

0.0 

33 

0.0 

0.0 

1565 

N1533 

N1533 

64 

0.0 

74 

0.0 

0.0 

1587 

*  A 1498 

*  A 1498 

37 

24.3 

40 

15.0 

19.5 

1588 

*  A 1492 

*  A 1492 

44 

2.3 

44 

0.0 

1.1 

1626 

N1565 

N1565 

25 

0.0 

32 

0.0 

0.0 

1668 

A 1587 

A 1588 

43 

2.3 

69 

2.9 

2.7 

1687 

A 1587 

N1587 

55 

1.8 

63 

12..7 

7.6 

1701 

N1626 

N1626 

77 

0.0 

68 

0.0 

0.0 

1722 

N1668 

N1668 

30 

0.0 

70 

4.3 

3.0 

1785 

N1687 

A 1687 

29 

10.3 

33 

152 

12.9 

1787 

N1701 

N1701 

32 

0.0 

40 

0.0 

.0 

1A     /* 

1788 

A 1668 

N1668 

5 

0.0 

80 

11.3 

10.6 

1830 

N1787 

N1787 

45 

0.0 

sS 

0.0 

0.0 

*7      O 

1857 

N1722 

N1722 

20 

10.0 

62 

6.4 

1  t  \ 

1859 

A 1785 

N1785 

21 

0.0 

30 

33.3 

19. b 

0.0 

12.9 

0.0 
9.7 

0.0 
31   T 
21 
28 

5  8 

0.0 

0.0 
'.0 

1890 

N1830 

N 1830 

7 

0.0 

8 

0.0 

1961 

N1859 

A 1859 

49 

16.3 

44 

9.1 

2006 

N1788 

A 1788 

18 

5.6 

40 

25.0 

2013 

N1890 

N1890 

12 

0.0 

16 

0.0 

2084 

A 1857 

A 1857 

8 

12.5 

23 

8.7 

0.0 

39.3 

33.3 

30.0 

0.0 

43.8 

0.0 

0.0 

90 

0.0 

100.0 

2194 

N2013 

N2013 

18 

0.0 

9 

2224 
2226 
2296 
2313 
2366 

A 1961 
A 1961 
A  2084 
N2194 
A  2296 

A  2006 
A  2006 
A  2084 
N2194 
A  2224 

13 
68 
25 
14 
8 

15.4 
10.3 
28.0 
0.0 
50.0 

28 
99 
10 
23 
16 

2367 

N2313 

N2313 

11 

0.0 

15 

01 

2458 
2471 

N2367 
A  2366 

N2367 
A  2366 

24 

78 

0.0 
79.5 

21 

114 

46 

'.1 

2503 
2524 

N2458 
A  2471 

N2458 
A  2471 

53 
45 

0.0 
100.0 

•From  wild  material  (see  page  13). 


THE  EFFECT  OF  SEXUAL  SELECTION.* 


It  is  relatively  easy  to  get  by  artificial  selection  a  strain  of  Drosophila 
ampelophila  in  which  practically  all  the  individuals  possess  extra  wing- 
veins.  Also,  by  selection  one  can  reduce  the  amount  of  venation.  The 
latter  strain  is  manifestly  not  fitted  to  maintain  itself,  because  the  wings, 
deprived  of  the  support  of  the  veins,  droop  and  catch  in  the  food  of  the 
insect,  resulting  in  the  insect's  death.  On  the  other  hand,  the  wings 
of  the  extra- veined  race  are  strong,  the  individuals  are  vigorous  and  fer- 
tile. What  would  be  the  fate  of  such  a  race  if  turned  loose  in  nature 
(a)  where  they  would  find  plain-winged  individuals  with  which  to  breed 
and  (6)  where  they  were  isolated  from  plain-winged  individuals?  Rea- 
soning from  the  fate  of  most  feral  domestic  races,  one  would  expect 
that  in  the  former  case  they  would  soon  disappear,  although  the  reason 
assigned  for  their  disappearance  would  be  the  vague  one  that  they 
would  be  ''swamped."  In  the  latter  case  many  would  expect  them  to 
keep  the  domestic  characteristics. 

Two  cubic  feet  of  space  and  a  few  decaying  bananas  form  conditions 
sufficiently  feral  for  the  purpose  of  testing  what  would  happen.  On 
May  2  I  released 'in  a  large  battery-jar  an  equal  number  of  flies  from  one 
of  my  extra-veined  strains  and  from  one  of  my  plain-winged  strains. 
This  would  clearly  give  the  extra-veined  an  advantage,  for  not  often  will 
a  new  form  make  up  50  per  cent  of  the  population.  On  May  19  only  26 
per  cent  of  the  flies  in  the  jar  showed  extra  veins  and  these  veins  were 
not  as  pronounced  as  those  of  the  original  50  per  cent.  By  May  26  the 
number  was  reduced  to  11  per  cent.  It  was  7  per  cent  on  June  9,  and  two 
weeks  later  (June  23)  only  1  per  cent  showed  any  trace  of  extra  veins. 

On  February  19  I  released  in  a  similar  jar  a  population  of  flies  selected 
from  an  extra-veined  race  on  the  basis  of  well-developed  extra  veins. 
No  plain-winged  flies  were  introduced.  However,  after  six  weeks 
(March  31)  only  93  per  cent  showed  extra  veins  and  in  none  of  these 
cases  were  the  extra  veins  very  strong.  On  April  24  there  were  only 
84  per  cent;  May  28,  72  per  cent;  June  23,  49  per  cent;  and  by  August 
3  only  5  per  cent  showed  any  trace  of  extra  veins. 

As  has  been  shown,  plain-winged  individuals  occasionally  turn  up  in 
carefully-bred  extra-veined  races,  but  it  was,  at  first,  puzzling  to  see  how 
these  occasional  "reversions"  could  get  such  a  foothold  as  to  supplant 
the  extra- veined  flies  which  were  in  the  j  ar  by  the  hundreds.  The  expla- 
nation was  found  while  testing  the  selective  value  of  the  prominent  male 
secondary  sexual  character  on  the  anterior  tibiae— the  large  tibial  comb. 

*Paper  read  before  the  American  Society  of  Naturalists,  Boston  meeting,  1909. 
36 


THE  EFFECT  OF  SEXUAL  SELECTION.  37 

I  cut  them  off  of  a  plain-winged  male  and  left  them  on  a  male  of  the 
extra-veined  race  and  vice  versa.  These  two  males  were  then  given  to 
a  female  as  mates.  By  a  study  of  her  offspring  I  could  tell,  in  a  rough 
way,  which  mate  she  preferred.  To  my  surprise  she  chose  almost  exclu- 
sively the  normal  male,  whether  he  had  tibial  adornments  or  not. 

Then,  without  removing  the  tibial  combs,  I  gave  plain-winged  and 
extra-veined  individuals  the  choice  between  mates  which,  as  far  as  I 
could  determine,  were  alike  in  all  particulars  such  as  age,  nutrition, 
activity,  and  time  since  last  copulation,  but  differed  in  that  one  had 
extra  veins  while  the  other  had  not.  I  watched  each  experiment  until 
copulation  had  taken  place.  When  the  extra  venation  in  one  mate  was 
great,  the  chooser,  whether  male  or  female,  normal  or  extra-veined, 
chose  the  normal  mate.  I  then  tried  weaker  degrees  of  the  character  and 
in  85  experiments,  mostly  with  flies  having  the  extra  veins  only  very 
slightly  developed,  61  of  the  choices  were  in  favor  of  the  wild  type. 

The  basis  upon  which  these  flies  discriminate  against  extra-veined 
individuals  when  choosing  a  mate  is  a  matter  for  further  study.  There 
is  an  elaborate  "courtship,"  in  which  the  flirting  of  the  wings  in  front 
of  the  prospective  mate  plays  a  large  part.  It  seems  as  though  a  choice 
were  made  on  the  basis  of  sight,  but  I  doubt  whether  that  is  the  case. 
However,  there  is  no  doubt  of  the  choice.  It  is  a  clear  case  of  the 
undoing  of  artificial  selection  by  sexual  selection. 


DISUSE  AND  DEGENERATION. 


* 


One  of  the  several  much-discussed  but  little-tested  problems  of  the 
theory  of  evolution  is  that  of  the  inherited  effects  of  disuse.  I  believe  that 
there  is  a  pretty  general  idea  that  when  a  species  no  longer  has  need  for 
an  organ  that  organ  will  degenerate.  The  explanations  of  this  degener- 
ation are  varied,  but  the  most  popular  seem  to  be  the  inheritance  of 
acquired  characters,  panmixia  and  selection.  It  is  indisputable  that  in 
the  life  of  an  individual  many  unused  organs  do  degenerate,  but  it  is  far 
from  proven  or  even  satisfactorily  indicated  that  this  ontogenetic  degen- 
eration is  followed  by  a  phylogenetic  degeneration.  There  is  no  doubt 
that  many  degenerate  organs  are  not  used  in  any  way;  but  who  can  say 
whether  this  disuse  has  preceded  degeneration  as  a  cause  or  merely  fol- 
lowed as  a  necessary  consequence  ?  Before  attempting  to  explain  the 
phylogenetic  degeneration  which  follows  disuse  it  seems  desirable  to  find 
a  clear  case  of  such  a  sequence,  and  this  quest  was  the  purpose  of  the 
experiment  with  Drosophila  ampelophila  upon  which  I  wish  briefly  to 
report. 

These  insects  are  normally  very  good  fliers,  possessing  wings  which 
are  relatively  quite  large.  In  my  experiments,  however,  they  were  con- 
fined in  glass  vials  barely  large  enough  to  contain  the  food.  The  only 
opportunity  they  had  to  fly  was  when  they  were  transferred  from  one 
vial  to  another.  This  was  done  only  three  times  a  week.  Such  flight 
could  at  most  not  be  more  than  5  cm.,  and  was,  as  a  matter  of  fact, 
rarely  made,  as  they  usually  walked. 

The  experiments  are  complicated  by  several  facts  which  must  be  con- 
sidered.    These  fall  into  two  groups: 

First,  those  which  might  explain  the  absence  of  degeneration  in  the 
wings.  Disuse  does  not  affect,  during  the  life  of  an  individual,  the 
wing-dimensions,  for  after  an  insect's  wings  are  expanded  there  is  no 
change  in  them  and,  of  course,  they  are  not  subject  to  the  effects  of  use 
and  disuse  before  they  are  expanded.  However,  the  degeneration  of 
beetle- wings  when  the  elytra  are  fused,  of  the  wings  of  cave  insects,  of 
parasites,  and  of  the  wings  of  many  female  Lepidoptera  are  used  as  stock 
examples  of  disuse.  Furthermore,  if  there  be  anything  in  the  theory 
of  hormones  (of  which  Cunningham  has  recently  made  so  much)  or  the 
various  forms  of  the  memory  theory  of  inheritance,  we  would  expect 
phylogenetic  degeneration  because  of  the  germ-plasm  receiving  the  news 
that  the  wings  are  not  being  used,  providing  the  plasm  is  in  condition  to 

*Paper  read  before  the  American  Society  of  Zoologists,  Baltimore  meeting,  1908. 
38 


DISUSE  AND  DEGENERATION.  39 

receive  and  act  upon  such  a  stimulus.  In  certain  insects  the  germ-cells 
are  all  practically  matured  before  or  by  the  time  the  wings  are  expanded 
and  ready  for  use.  This,  however,  is  not  the  case  with  Droaophila. 
Not  only  are  the  germ-cells  not  all  matured  by  the  time  it  becomes  adult, 
but  they  are  in  all  stages  of  development  and  continue  to  mature,  a  : 
at  a  time,  for  a  month  thereafter.  In  these  experiments  I  rarely  u 
as  parents  the  individuals  coming  from  first-laid  eggs,  so  that  there  were 
strong  chances  of  my  using  affected  germ-plasm  if  such  exists.  Any 
experiment,  such  as  this,  is  always  open  to  the  criticism  that  it  has  not 
been  sufficiently  long  continued,  but  I  am  sure  that  most  will  agree 
that  43  generations,  combined  with  microscopic  measurements  and  the 
delicacy  of  biometric  analysis,  ought  to  give  a  satisfactory  indication  of 
what  is  taking  place. 

The  second  set  of  considerations  might  explain  any  observed  degen- 
erations without  reference  to  the  disuse.  Excessive  inbreeding  was 
practiced,  sister  usually  being  bred  to  brother.  This  was  necessary  f  <  >r, 
if  I  had  planned  to  stop  at  this  point  and  had  wished  to  entirely  avoid 
inbreeding,  I  would  have  needed  more  than  8  trillion  flies  with  which  to 
start  the  work.  Inbreeding  is  supposed  to  lead  to  degeneration  and  might 
thus  be  solely  accountable  for  degeneration,  or  it  might  assist  disuse. 
Unnatural  conditions  might  have  adversely  affected  the  flies.  Confine- 
ment itself,  apart  from  the  entailed  disuse,  might  at  least  help  to  bring 
about  degeneration.  Furthermore,  I  kept  the  insects  breeding  winter 
and  summer,  with  no  rest  for  hibernation  and  with  no  change  of  food. 
There  was  no  conscious  selection  favoring  perfect  and  large  wings,  as 
all  measurements  of  this  strain  were  made  quite  recently  and  the  vari- 
ations in  wing-dimensions  are  not  readily  appreciable,  hence  the  removal 
of  selection  in  favor  of  good  wings  might  result  in  panmixia  and  conse- 
quent degeneration.  Finally,  I  was  constantly  on  the  lookout  for  signs 
of  degeneration,  as  I  hoped  and  still  do  hope  to  produce  a  wingless  Dro- 
sophila.  My  desire  might  have  influenced  my  actions  and  an  unconscious 
selection  on  my  part  might  have  reduced  the  size  of  the  wings  without 
disuse  playing  a  part. 

The  only  necessary  answer  to  this  second  set  of  considerations  is  that, 
in  spite  of  the  possibility  of  the  degenerating  effect  of  disuse  being  helped 
by  inbreeding,  unnatural  conditions,  panmixia,  or  selection,  there  has 
been  no  degeneration. 

Evidence  of  degeneration  was  sought  for  by  carefully  measuring  the 
expanded  wings  of  the  individuals  belonging  to  successive  stages  of  the 
experiment.    In  making  these  measurements  one  may  not  mix  the  sa 
because  of  the  sexual  difference  in  size.      Therefore  the  females  al< 
were  used,  since  among  insects  it  is  more  commonly  the  females  which 
have  degenerate  wings.     The  results  are  shown  in  table  37.  where 
units  of  length  equal  1  mm. 


40  EXPERIMENTS  WITH  DROSOPHILA  AMPELOPHILA. 

Table  37. — Mean  wing-dimensions  at  various  periods  of  continued  disuse. 


Generations  of  disuse. 

Length  of  wing. 

Breadth  of  wing. 

Length  X  breadth. 

1st  to  3rd 

67.00  ±0.12 
66.50  ±0.11 
64.91  ±0.12 
67.67  ±0.18 

32.55  ±0.07 
33.60  ±  0.06 
31.98  ±0.06 
34.06  ±0.08 

2223.12  ±   8.85 
2281.12  ±    7.41 
2115.44  ±    7.42 
2358.94  ±11.46 

17th  to  19th  

33rd  to  35th 

41st  to  43rd 

If  the  experiment  had  stopped  at  the  end  of  the  thirty-fifth  generation 
it  would  have  appeared  from  this  table  that  the  wings  were  actually- 
getting  smaller,  since  the  area,  as  judged  by  length  X  breadth,  was 
smaller  in  the  second  lot  than  in  the  first,  and  still  smaller  in  the  third — 
the  difference  being  nearly  ten  times  the  expected  error.  However,  this 
would  have  been  a  hasty  conclusion.  The  fourth  lot  is  as  much  larger 
than  the  first  as  the  third  is  smaller.  So  we  must  conclude  that  there 
is  no  evidence  that  the  constant  disuse  of  the  wings  during  more  than 
40  generations  has  had  any  effect. 


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